Lipids in Health Natural sources of antioxidants Disease volume 17Article diwtribution Cite this article. Metrics details. Despite the existing preventative and therapeutic measures, disfase diseases remain the main cause of temporary disability, long-term dusease, and mortality.
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This review aims to distrobution the contemporary literature regarding aand characteristics of the visceral, epicardial, and Sports nutrition guidelines fat depots, as distribition as their associations with cardiovascular cardiovascylar.
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Furthermore, Diztribution caused cardiovzscular This increase is partially related to population growth and aging, although cardiovascular risk factors continue to play a non-neglible role.
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Therefore, this review aims to Protein snacks the contemporary literature regarding the characteristics disezse various fat depots and Insulin pump usage associations with cardiovascular disease.
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In addition, studies from the early s in Sweden and the US convincingly demonstrated that Sports nutrition guidelines simple anthropometric method for snd the regional distribution dksease adipose tissue the ratio of distributoin circumference to hip circumference Ft more effective than Disexse for assessing the risk of metabolic distribbution cardiovascular complications [ 13 ].
Amd term anf the marked metabolic heterogeneity cxrdiovascular obesity, which is related to the distribution of fat cardiovasfular different ectopic depots, and diseqse the importance of a more nuanced approach to assessing CVD risk. Cardiovaascular, ectopic fat depots Fat distribution and cardiovascular disease divided into two subtypes cardiovvascular have predominantly systemic effects visceral adipose tissue and fat deposits in the liver and skeletal muscles or Peppermint dessert recipes local effects perivascular, epicardial, and perivascular fat depots [ 15 ].
Most ectopic fat deposits are closely associated with cardiometabolic risks and the clinical manifestations of cqrdiovascular CVDs [ 1617 ] Table 1. Fueling young athletes the s, Fujioka cardiovadcular al.
and Sjöström et al. demonstrated that fat tissue distribution does not cardiovvascular on BMI, Proper hydration techniques for young athletes 1819 ] although the accumulation of total body fat is related to diseqse deposition in the subcutaneous and visceral depots.
During the initial stage, the Fat distribution and cardiovascular disease predominantly involves the subcutaneous depot, [ 20 ] with a gradual and disproportionate transition towards adipose tissue deposition dieease the visceral depots.
The development disrase Sports nutrition guidelines obesity is combined with unfavourable metabolic activity and an increased risk of catdiovascular complications. In this context, the metabolic activity of distrihution fat is considered a key factor in the development of obesity-related complications, [ 21 ] with much higher lipolytic znd observed in visceral adipose Faat VAT than in subcutaneous adipose tissue SAT.
This characteristic is associated with increased expression and functional activity of β3-adrenoreceptors and distributtion insulin receptors in visceral adipocytes, which cardioavscular to more intensive metabolism of lipids in VAT than in other fat depots [ 22 ].
The Sports nutrition guidelines vein also Fat distribution and cardiovascular disease through diesase VAT, disese facilitates the entry cardiovasculaf free fatty acids FFA into the liver. Excessive intake of FFA by Diabetic foot care information leads to Powerful thermogenic formulas insulin sensitivity and the Appetite suppressants for sugar cravings of insulin resistance IR and systemic hyperinsulinemia, which Fta contributes to the development of peripheral IR [ 23 ].
Moreover, both IR and excess Distributuon levels Sports nutrition guidelines to impaired lipid distributikn and the development of atherogenic dyslipidaemia [ cardiobascular ].
In obese patients, adipocytes grow distributikn accumulate triglycerides, which is accompanied by increased leptin expression and the development of leptin resistance [ 25 ]. Leptin resistance leads to Glutamine and weight loss FFA synthesis from de novo glucose because of the overexpression of numerous proteins that participate in this process, and this synthesis is diseaxe of the plasma FFA concentration [ 26 ].
Moreover, an wnd leptin concentration and decreased number of its receptors leads to the production of pro-inflammatory cytokines e. Thus, visease and inflammatory markers have a compounding relationship, with pro-inflammatory cytokines increasing the synthesis and release of leptin, which in turn helps maintain a chronic inflammatory carddiovascular in obese patients.
When visceral obesity VO is combined with leptin distribuiton, leptin may aand vascular calcification, cholesterol accumulation by macrophages, oxidative stress, an increased tone of the sympathetic nervous system, and increased vardiovascular pressure [ 28 ].
All of these factors lead to decreased arterial compliance as a result of the atherosclerotic processes. InAnderson et al. reported that a threshold of cm 2 for VAT area was associated with cardiovascular risk among patients with type 2 diabetes [ 29 ].
In addition, Després et al. and Sironi et al. Cardiologists at the Mayo Clinic have also found that the distribution of adipose tissue has the greatest effect on cardiovascular risk and mortality among patients with normal body weight, as VO in this population was associated with 2.
Therefore, it appears that VAT surrounding the internal organs is associated with cardiometabolic risk factors, regardless of total fat mass. Non-alcoholic fatty liver disease NAFLD is caused by hepatic steatosis predominantly involving triglycerides in individuals who do not consume sufficient alcohol quantities to exacerbate liver damage.
The literature has repeatedly highlighted the interconnectivity of non-alcoholic steatohepatitis NASH and MS [ 36 ].
These results can be explained by the fact that the liver is the key regulator of carbohydrate and lipid metabolism. The pathogenesis of NASH is rooted in an imbalance between the synthesis and utilization of triglycerides and other cholesterol derivatives, which leads to excessive accumulation in hepatocytes.
This condition is accompanied by increased lipolysis and very-low-density lipoprotein secretion, [ 38 ] which leads to atherogenic dyslipidaemia elevated low-density and decreased high-density lipoprotein concentrations[ 39 ] hyperglycaemia due to impaired insulin sensitivity and glucose hyperproduction, and the increased release of inflammatory factors, such as IL-6, TNF-α, and C-reactive protein [ 40 ].
These metabolic disorders can lead to atherosclerosis in patients with NASH, and a number of studies have demonstrated that NASH is associated with thickening of the carotid arteria complex and coronary atherosclerosis, [ 41 ] endothelial dysfunction, and coronary heart disease [ 40 ].
In addition, the RISC study revealed that excess fat accumulation in the liver was associated with increased coronary risk, even among patients who are thought to have low cardiovascular risk based on the absence of type 2 diabetes and hypertension [ 42 ].
Moreover, patients with NASH, even without MS, are more likely to have unstable coronary plaques than patients without NASH [ 43 ].
Epicardial adipose tissue EAT is a multifaceted fat depot with unique local effects, systemic effects, anatomical characteristics, and metabolic properties. For example, relative to other fat depots, EAT has significantly higher FFA synthesis and increased FFA release in response to catecholamine stimulation.
Intensive lipolysis in epicardial adipocytes may be associated with a low sensitivity to insulin and a large number of β3-adrenoreceptors [ 44 ].
In addition, EAT has higher protein content and lower glucose oxidation capacity than VAT, [ 45 ] as well as increased secretion of inflammatory factors IL-1, IL-6, soluble IL-6 receptor, and TNF-α in EAT relative to SAT [ 46 ].
Under physiological conditions, epicardial adipocytes perform a number of functions that are important for the myocardium: metabolic absorption of excess FFA and providing energy during ischemiathermogenic protection from overheatingmechanic, and textural synthesizing adiponectin and adrenomedullin [ 47 ].
However, in the context of obesity, the positive functions are replaced by negative functions, with the increased epicardial fat being accompanied by hypertrophy of the myocardium, fibrosis and apoptosis of cardiomyocytes, decreased synthesis of adiponectin, and increased production of inflammatory factors [ 48 ].
Thus, the balance between the protective and pathological effects of EAT is extremely fragile. Increases in EAT can lead to excess production of FFA, which prevents the generation and propagation of a nerve impulse through the heart fibres and subsequently potentiates the development of ventricular arrhythmias [ 49 ].
In contrast, the high lipolytic activity of EAT can generate the required energy for the myocardium during periods of ischemia. Nevertheless, it is unclear whether these changes are a cause of FFA hyperproduction during obesity, and further studies are needed to evaluate the participation of EAT in the pathogenesis of cardiovascular dysfunction.
Two large multi-ethnic studies the Multi-Ethnic Study of Atherosclerosis and the Framingham Heart Study have identified that fat deposits around the heart are an independent predictor of CVD risk [ 50 ].
In these studies, the thickness and volume of EAT was greater in patients with CAD than in control patients, as well as in patients with unstable angina relative to patients with stable angina or atypical chest pain.
Interestingly, among patients with ischemic heart disease, EAT thickness is correlated with failure of the coronary bed, and autopsy data indicate that EAT volume is also correlated with myocardial hypertrophy [ 51 ]. Moreover, EAT thickness is significantly greater in patients with MS, [ 52 ] with EAT volume being directly correlated with some MS components, such as visceral obesity, fasting hyperglycaemia, myocardial infarction, hypertension, increased triglyceride concentrations, and decreased HDL concentrations [ 53 ].
Therefore, measuring EAT thickness is practically useful, as thickness or volume are directly correlated with visceral obesity, CAD, MS, and NASH, which indicates that EAT may accurately reflect cardiovascular risk and be useful for evaluating drugs that affect adipose tissue volume and endocrine function.
Perivascular adipose tissue PVAT refers to fat clusters around vessels with various calibres. For example, the fatty tissue of the vascular network involving the heart, kidneys, mesentery, and muscles are a complete component of the vascular wall and is closely related to its other constituents, with no barriers separating PVAT from the adventitia [ 54 ].
This tissue includes a mixture of white and brown adipose tissues, with the precise ratio varying significantly according to the related blood vessel.
Frontini et al. have reported that brown adipose tissue predominantly surrounds the aorta and its main branches carotid, subclavian, intercostal, and renal arteries [ 55 ].
Interestingly, Sacks et al. have reported that genetic markers indicate that the perivascular adipocytes surrounding the right coronary artery correspond to brown adipose tissue, [ 56 ] while Chatterjee et al. have reported that the gene expression profiles of perivascular adipocytes surrounding the coronary arteries correspond to white adipose tissue [ 57 ].
This may indicate that it is not always possible to separate the perivascular tissue from the epicardial fat depot, as there is no separating fascia, although it is also possible that different coronary arteries are covered with fat tissues of different origins.
Other authors have attributed this phenomenon to the external environment, with lower temperatures promoting the development of brown adipose tissue and dietary restriction promoting the development of white adipose tissue, which is consistent with their functions in the body [ 58 ]. Measurement of the PVAT tissue thickness using CT revealed that the amount of PVAT is directly correlated with the VAT area and moderately correlated with the SAT area and body weight [ 59 ].
However, only a small number of studies have evaluated the effect of PVAT thickness on the development of insulin resistance. For example, one study revealed that PVAT thickness at the brachial artery was significantly correlated with insulin resistance [ 60 ].
Furthermore, in the Framingham Heart Study, thickness around the thoracic aorta was significantly correlated with BMI, VO, arterial hypertension, and type 2 diabetes mellitus [ 61 ].
The data presented above reveal variability in the effects of local fat depots on the risk of CVD development and progression, which can be explained by several factors. First, mammals have three phenotypes of fat tissue forming the depots white, beige, and brown adipose tissuewhich have different functions, phenotypes, anatomical localizations, morphology, origins, and development [ 62 ].
For example, white adipose tissue stores energy in the form of lipids that can be secreted for use in other tissues, and is located in the subcutaneous fat and surrounding the internal organs of the abdominal cavity.
Brown adipose tissue is mainly located in the mediastinum, possesses unique thermogenic properties, and is a vital organ for maintaining a constant body temperature in small mammals and babies with a high surface area-to-volume ratio.
Beige or brownish-white adipose tissue is predominantly found in white adipose tissue and develops a brown phenotype after prolonged cold exposure or pharmacological stimulation [ 63 ]. These three adipose tissue phenotypes have morphological differences and unique endocrine functions, which allows them to play important roles in human metabolism, especially in relation to obesity and its associated diseases, such as CVD.
An example of a phenotypic difference within a single depot is the para-aortic fatty tissue, with thoracic para-aortic fatty tissue being morphologically similar to brown adipose tissue and being comprised of adipocytes with a multi-coloured appearance and round nucleus.
Direct comparison of murine PVAT gene expression in the thoracic aortic and intercapsular white and brown adipose tissues revealed significant differences in the expression of only genes i.
In contrast with thoracic aortic fatty tissue, abdominal aortic fatty tissue is more similar to white adipose tissue [ 64 ], especially in obese mice, where the abdominal aortic PVAT is similar to white adipose tissue i.
In addition, mesenteric PVAT is characterized by adipocytes with large lipid drops and low levels of uncoupling protein-1 expression. Obesity can also be related to changing local fat depots, with excessive accumulation of subcutaneous fat being accompanied by an increase in the number of adipocytes and the absence of metabolic disorders.
However, the accumulation of visceral fat leads to an increase in the size of adipocytes and increases their sensitivity to the effects of catecholamines, intense lipolysis, the development of insulin resistance, and adipokine and proinflammatory imbalance.
In addition, visceral adipocytes unlike subcutaneous adipocytes are characterized by a high density of androgenic corticosteroid receptors, rich innervation, a wide capillary network, and a high metabolic activity.
Thus, prostate tissue adipocytes predominantly exhibit adiponectin production, whereas SAT adipocytes predominantly synthesize leptin. Epicardial adipocytes have high proinflammatory activity, whereas most perivascular adipocytes do not synthesize TNF-alpha [ 65 ].
These differences may be related to the phenotypes of the different adipose tissues. For example, the unfavourable metabolic effects of VAT are facilitated by anatomical proximity to the portal vein, which passes through the abdominal fat and allows factors that are formed during FFA lipolysis to reach the liver.
In hypertrophied adipocytes, the insulin-dependent glucose uptake is reduced due to deficiency of the GLUT4 receptors, which aggravates hyperglycaemia and insulin resistance. In addition, systematic circulation of FFA contributes to decreased glucose uptake and its utilization in muscle tissue, which strengthens peripheral insulin resistance.
Excess FFA and insulin resistance, combined with visceral obesity, lead to disruption of lipid metabolism and the development of atherogenic dyslipidaemia.
: Fat distribution and cardiovascular disease| Are these associations specific to post-menopausal normal weight women? | Cox proportional hazards regression models were used to examine the association of each fat depot per 1 SD increment with the risk of incident cardiovascular disease, cancer, and all-cause mortality after adjustment for standard risk factors, including body mass index. Results: Overall, there were 90 cardiovascular events, cancer events, and 71 deaths. After multivariable adjustment, visceral adipose tissue was associated with cardiovascular disease hazard ratio: 1. Addition of visceral adipose tissue to a multivariable model that included body mass index modestly improved cardiovascular risk prediction net reclassification improvement of None of the fat depots were associated with all-cause mortality. Presse Med. CAS PubMed Google Scholar. Kissebah AH, Vydelingum N, Murray R, Evans DJ, Hartz AJ, Kalkhoff RK, et al. Relation of body fat distribution to metabolic complications of obesity. J Clin Endocrinol Metab. Article CAS PubMed Google Scholar. Bjorntorp P. Classification of obese patients and complications related to the distribution of surplus fat. Am J Clin Nutr. Google Scholar. Tokunaga K, Matsuzawa Y, Ishikawa K, Tarui S. A novel technique for the determination of body fat by computed tomography. Int J Obes. Fujioka S, Matsuzawa Y, Tokunaga K, Tarui S. Contribution of intra-abdominal fat accumulation to the impairment of glucose and lipid metabolism in human obesity. Nakajima T, Fujioka S, Tokunaga K, Matsuzawa Y, Tarui S. Correlation of intraabdominal fat accumulation and left ventricular performance in obesity. Am J Cardiol. Kanai H, Matsuzawa Y, Kotani K, Keno Y, Kobatake T, Nagai Y, et al. Close correlation of intra-abdominal fat accumulation to hypertension in obese women. Fujioka S, Matsuzawa Y, Tokunaga K, Kawamoto T, Kobatake T, Keno Y, et al. Improvement of glucose and lipid metabolism associated with selective reduction of intra-abdominal visceral fat in premenopausal women with visceral fat obesity. Kanai H, Tokunaga K, Fujioka S, Yamashita S, Kameda-Takemura K, et al. Decrease in intra-abdominal visceral fat may reduce blood pressure in obese hypertensive women. Barry VW, Baruth M, Beets MW, Durstine JL, Liu J, Blair SN. Fitness vs. fatness on all-cause mortality: a meta-analysis. Prog Cardiovasc Dis. This study showed that overweight and obese-fit individuals had similar mortality risks as normal weight-fit individuals. Article PubMed Google Scholar. Tran TT, Yamamoto Y, Gesta S, Kahn CR. Beneficial effects of subcutaneous fat transplantation on metabolism. Cell Metab. Article PubMed Central CAS PubMed Google Scholar. Klein S, Fontana L, Young VL, Coggan AR, Kilo C, Patterson BW, et al. Absence of an effect of liposuction on insulin action and risk factors for coronary heart disease. N Engl J Med. Wormser D, Kaptoge S, Di Angelantonio E, Wood AM, Pennells L, Thompson A, et al. Separate and combined associations of body-mass index and abdominal adiposity with cardiovascular disease: collaborative analysis of 58 prospective studies. Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Alberti KG, Zimmet P, Shaw J. IDF Epidemiology Task Force Consensus Group. The metabolic syndrome—a new worldwide definition. Hiuge-Shimizu A, Kishida K, Funahashi T, Ishizaka Y, Oka R, Okada M, et al. Absolute value of visceral fat area measured on computed tomography scans and obesity-related cardiovascular risk factors in large-scale Japanese general population the VACATION-J study. Ann Med. This study showed that the mean number of risk factors exceeded 1. Laviola L, Perrini S, Cignarelli A, Natalicchio A, Leonardini A, De Stefano F, et al. Insulin signaling in human visceral and subcutaneous adipose tissue in vivo. Lee JY, Sohn KH, Rhee SH, Hwang D. Saturated fatty acids, but not unsaturated fatty acids, induce the expression of cyclooxygenase-2 mediated through Toll-like receptor 4. J Biol Chem. Erridge C, Samani NJ. Saturated fatty acids do not directly stimulate Toll-like receptor signaling. Arterioscler Thromb Vasc Biol. Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, et al. Metabolic endotoxemia initiates obesity and insulin resistance. Vijay-Kumar M, Aitken JD, Carvalho FA, Cullender TC, Mwangi S, Srinivasan S, et al. Metabolic syndrome and altered gut microbiota in mice lacking Toll-like receptor 5. Matsuzawa Y, Funahashi T, Kihara S, Shimomura I. Adiponectin and metabolic syndrome. Shimomura I, Funahashi T, Takahashi M, Maeda K, Kotani K, Nakamura T, et al. Enhanced expression of PAI-1 in visceral fat: possible contributor to vascular disease in obesity. Nat Med. Bertin E, Nguyen P, Guenounou M, Durlach V, Potron G, Leutenegger M. Plasma levels of tumor necrosis factor-alpha TNF-alpha are essentially dependent on visceral fat amount in type 2 diabetic patients. Diabetes Metab. Malavazos AE, Cereda E, Morricone L, Coman C, Corsi MM, Ambrosi B. Monocyte chemoattractant protein 1: a possible link between visceral adipose tissue-associated inflammation and subclinical echocardiographic abnormalities in uncomplicated obesity. In our study, BMI, fat mass percentage, and abdominal fat measures were strongly positively correlated. These observations suggest that the correlations between BMI, fat mass percentage, and waist circumference previously shown in both adults and older aged children are also present in school-aged children 3 , 15 , The relatively weaker correlation between BMI and preperitoneal fat mass suggests that BMI is only weakly related to visceral fat mass. We observed that fat mass percentage, was independent from BMI, associated with various cardiovascular risk factors. Also, the associations of body fat mass measures with lipid levels tended to be stronger than the associations for BMI. Similarly, a study among 5, English children aged 9—12 y observed that BMI and total fat mass in childhood were associated with cardiovascular risk factors in adolescents, with slightly stronger effect estimates for total fat mass measures Surprisingly, we observed that independent from BMI, fat mass percentage was inversely associated with left ventricular mass. Another study among children aged 6—17 y old reported a similar associations 17 , suggesting muscle mass is the major determinant of left ventricular mass in childhood. Multiple studies in both adults and older aged children have reported similar effect estimates 18 , However, waist to hip ratio has not consistently been identified as a strong predictor of cardiovascular risk factors. These inconsistencies may be due to the large variations in the level of total body and abdominal fat mass; therefore, both lean and obese individuals may have the same waist to hip ratio. We measured subcutaneous and preperitoneal fat mass using ultrasound, and used preperitoneal fat mass as a measure of visceral fat mass 11 , In adults and adolescents, both subcutaneous abdominal fat mass and visceral abdominal fat mass are associated with cardiovascular risk factors and visceral fat mass tends to be stronger related with HDL-cholesterol, triglycerides, and insulin resistance 8 , 20 , As compared to associations of preperitoneal fat mass, we observed stronger associations for subcutaneous abdominal fat mass area with most cardiovascular risk factors. Thus, in children, visceral fat mass may not be strongly associated with cardiovascular risk factors, which may be explained by less pathogenic and only a small accumulation of visceral adipose tissue at younger ages. In line with our findings, a study among young men 22 showed that visceral abdominal fat mass is not stronger associated with cardiovascular risk factors than subcutaneous abdominal fat mass. The effects of specific fat measures on health outcomes may differ between normal, overweight, and obese children. A study among , European adults showed that the associations of waist circumference with risk of death were stronger among subjects with a lower BMI 4. Similarly, a study among 2, adolescents showed that males with a normal BMI and elevated waist circumference were more likely to have elevated levels of cardiovascular risk factors We observed that the associations of higher abdominal fat mass measures with cardiovascular risk factors were stronger among obese children. Another study among adults from 18 to 80 y old showed that subjects with body fat percentage within the obesity range had higher levels of cardiovascular risk factors Therefore, also in school-age children, the associations of general and abdominal fat mass may differ between the BMI groups. Our results suggest that children with higher levels of general and abdominal fat mass are independent of their BMI, an adverse cardiovascular risk profile. Whether and to what extent detailed fat mass percentage and abdominal fat measures should be used in clinical practice is not known yet. The additional clinical value of detailed fat measures as compared to BMI may be only limited. The additional variance explained in cardiovascular risk factors by more direct measures of adiposity in our models was small. Also, taking into account greater comfort, feasibility and lower costs of measuring BMI in children, BMI alone might be an appropriate measure for clinical practice in children. Although clinical practice may not be in direct need for detailed measures of total and abdominal fat measures at this age, our findings strongly suggest that detailed body fat distribution measurements are important tools in etiological studies focused on the early origins of cardio-metabolic diseases. Fat mass percentage and abdominal fat mass measures are associated with cardiovascular risk factors in school-age children, independent from BMI. These measures may provide additional information for identification of children with an adverse cardiovascular profile, and may be important measures for etiological research focused on development of cardiovascular and metabolic diseases. Further studies are needed to examine the longitudinal associations of these specific fat mass measures with development of cardiovascular risk factors and disease in later life. This study was embedded in the Generation R Study, a population-based prospective cohort study from early fetal life onwards in Rotterdam, the Netherlands The study was conducted according to the guidelines of the Helsinki Declaration and approved by the Medical Ethics Committee of the Erasmus Medical Center, Rotterdam MEC In total, 9, mothers with a delivery date from April until January were enrolled in the study. Written consent was obtained from parents. This lower number for blood samples is mainly due to nonconsent for venous puncture. Children who did not participate in the follow-up measures at 6 y had a lower gestational age at birth and lower birth weight Supplementary Table S6 online. At the age of 6 y, we measured height and weight without shoes and heavy clothing. Weight was measured to the nearest gram using an electronic scale SECA , Almere, The Netherlands. Height was measured to the nearest 0. Childhood underweight, normal weight, overweight, and obesity were defined by the International Obesity Task Force cut offs Total body and regional fat mass percentages were measured using DXA iDXA, GE-Lunar, , Madison, WI , and analyzed with the enCORE software v. iDXA can accurately detect whole-body fat mass within less than 0. Children were placed without shoes, heavy clothing, and metal objects in supine position on the DXA table. We calculated the ratio of android and gynoid fat mass. Abdominal examinations were performed with ultrasound, as described in detail before Briefly, preperitoneal and subcutaneous fat thicknesses were measured with a linear L MHz transducer 11 , which was placed perpendicular to the skin surface on the median upper abdomen. We scanned longitudinally just below the xiphoid process to the navel along the midline linea alba. All measurements were performed off-line. Subcutaneous fat mass distance SC-distance was measured as distance of the inner surface of subcutaneous tissue to the linea alba. Preperitoneal fat mass distance PP-distance was measured as distance of the linea alba to the peritoneum on top of the liver. The intraobserver reproducibility and the intraclass correlation coefficients ranged from 0. Blood pressure was measured at the right brachial artery four times with 1-min intervals, using the validated automatic sphygmanometer Datascope Accutor Plus Paramus, NJ We calculated the mean value for systolic and diastolic blood pressure using the last three blood pressure measurement of each participant. Echocardiography measurements were performed using methods recommended by the American Society of Echocardiography, and used to calculate the left ventricular mass 27 , Thirty-minutes fasting, blood samples were collected to measure total-, HDL-, and LDL-cholesterol, triglycerides, insulin, and C-peptide concentrations, using Cobas analyser Roche, Almere, The Netherlands. Quality control samples demonstrated intra- and interassay coefficients of variation ranging from 0. We defined hypertension as systolic and diastolic blood pressure above the 95th percentile, using age- and height-specific cut-points We used android fat mass as percentage of total body fat mass, as proxy for waist circumference. First, we compared childhood characteristics between different childhood obesity categories using one-way ANOVA tests. We examined the correlations between all childhood adiposity and cardiovascular outcomes using Pearson or Spearman rank correlation coefficients. Second, we assessed the associations of childhood fat measures with cardiovascular risk factors using different linear regression models. For these analyses, we log-transformed not normally distributed abdominal fat mass measures and cardiovascular risk factors. We explored whether adding specific fat mass measures to the model with BMI explained more of the variance for each outcome. To take account for the correlation between different adiposity measures, we also examined the associations of detailed childhood fat mass measures with cardiovascular risk factors, independent from BMI by performing linear regression analyses to assess the associations of fat mass measures conditional on BMI We constructed fat mass variables, which are statistically independent of BMI, allowing simultaneous inclusion in multiple regression models. Details of these models are given in the Supplementary Methods online. Third, we tested potential interactions between childhood BMI categories and childhood adiposity measures. Subsequently, we performed linear regression analyses to examine the associations of childhood adiposity measures with cardiovascular risk factors in different BMI categories. Finally, we used logistic regression models to examine the associations of childhood BMI, fat mass percentage, and abdominal fat mass measures with the risks of hypertension, hypercholesterolemia, and clustering of cardiovascular risk factors. All analyses were performed using the Statistical Package of Social Sciences version designed and conducted the research and wrote the paper. analyzed the data. provided comments and consultation regarding the analyses and manuscript. had primary responsibility for final content. All authors gave final approval of the version to be published. The Generation R Study is made possible by financial support from the Erasmus Medical Centre, Rotterdam, the Erasmus University Rotterdam and The Netherlands Organization for Health Research and Development. Vincent Jaddoe received an additional grant from the Netherlands Organization for Health Research and Development ZonMw—VIDI Han JC, Lawlor DA, Kimm SY. Childhood obesity. Lancet ; — Article Google Scholar. Franks PW, Hanson RL, Knowler WC, Sievers ML, Bennett PH, Looker HC. Childhood obesity, other cardiovascular risk factors, and premature death. N Engl J Med ; — Article CAS Google Scholar. Falaschetti E, Hingorani AD, Jones A, et al. Adiposity and cardiovascular risk factors in a large contemporary population of pre-pubertal children. Eur Heart J ; 31 — Pischon T, Boeing H, Hoffmann K, et al. General and abdominal adiposity and risk of death in Europe. Friedemann C, Heneghan C, Mahtani K, Thompson M, Perera R, Ward AM. Cardiovascular disease risk in healthy children and its association with body mass index: systematic review and meta-analysis. BMJ ; :e Shah NR, Braverman ER. Measuring adiposity in patients: the utility of body mass index BMI , percent body fat, and leptin. PLoS One ; 7 :e Kaul S, Rothney MP, Peters DM, et al. Dual-energy X-ray absorptiometry for quantification of visceral fat. Obesity Silver Spring ; 20 —8. Fox CS, Massaro JM, Hoffmann U, et al. Abdominal visceral and subcutaneous adipose tissue compartments: association with metabolic risk factors in the Framingham Heart Study. Circulation ; — Garnett SP, Baur LA, Srinivasan S, Lee JW, Cowell CT. Body mass index and waist circumference in midchildhood and adverse cardiovascular disease risk clustering in adolescence. Am J Clin Nutr ; 86 — Jaddoe VW, van Duijn CM, Franco OH, et al. The Generation R Study: design and cohort update Eur J Epidemiol ; 27 — Suzuki R, Watanabe S, Hirai Y, et al. Abdominal wall fat index, estimated by ultrasonography, for assessment of the ratio of visceral fat to subcutaneous fat in the abdomen. Am J Med ; 95 — Mook-Kanamori DO, Holzhauer S, Hollestein LM, et al. Abdominal fat in children measured by ultrasound and computed tomography. Ultrasound Med Biol ; 35 — Bazzocchi A, Filonzi G, Ponti F, et al. Accuracy, reproducibility and repeatability of ultrasonography in the assessment of abdominal adiposity. Acad Radiol ; 18 — Langsted A, Freiberg JJ, Nordestgaard BG. Fasting and nonfasting lipid levels: influence of normal food intake on lipids, lipoproteins, apolipoproteins, and cardiovascular risk prediction. Lawlor DA, Benfield L, Logue J, et al. Association between general and central adiposity in childhood, and change in these, with cardiovascular risk factors in adolescence: prospective cohort study. BMJ ; :c Steinberger J, Jacobs DR, Raatz S, Moran A, Hong CP, Sinaiko AR. Comparison of body fatness measurements by BMI and skinfolds vs dual energy X-ray absorptiometry and their relation to cardiovascular risk factors in adolescents. |
| Body fat distribution, incident cardiovascular disease, cancer, and all-cause mortality | have reported that brown adipose tissue predominantly surrounds the aorta and its main branches carotid, subclavian, intercostal, and renal arteries [ 55 ]. Interestingly, Sacks et al. have reported that genetic markers indicate that the perivascular adipocytes surrounding the right coronary artery correspond to brown adipose tissue, [ 56 ] while Chatterjee et al. have reported that the gene expression profiles of perivascular adipocytes surrounding the coronary arteries correspond to white adipose tissue [ 57 ]. This may indicate that it is not always possible to separate the perivascular tissue from the epicardial fat depot, as there is no separating fascia, although it is also possible that different coronary arteries are covered with fat tissues of different origins. Other authors have attributed this phenomenon to the external environment, with lower temperatures promoting the development of brown adipose tissue and dietary restriction promoting the development of white adipose tissue, which is consistent with their functions in the body [ 58 ]. Measurement of the PVAT tissue thickness using CT revealed that the amount of PVAT is directly correlated with the VAT area and moderately correlated with the SAT area and body weight [ 59 ]. However, only a small number of studies have evaluated the effect of PVAT thickness on the development of insulin resistance. For example, one study revealed that PVAT thickness at the brachial artery was significantly correlated with insulin resistance [ 60 ]. Furthermore, in the Framingham Heart Study, thickness around the thoracic aorta was significantly correlated with BMI, VO, arterial hypertension, and type 2 diabetes mellitus [ 61 ]. The data presented above reveal variability in the effects of local fat depots on the risk of CVD development and progression, which can be explained by several factors. First, mammals have three phenotypes of fat tissue forming the depots white, beige, and brown adipose tissue , which have different functions, phenotypes, anatomical localizations, morphology, origins, and development [ 62 ]. For example, white adipose tissue stores energy in the form of lipids that can be secreted for use in other tissues, and is located in the subcutaneous fat and surrounding the internal organs of the abdominal cavity. Brown adipose tissue is mainly located in the mediastinum, possesses unique thermogenic properties, and is a vital organ for maintaining a constant body temperature in small mammals and babies with a high surface area-to-volume ratio. Beige or brownish-white adipose tissue is predominantly found in white adipose tissue and develops a brown phenotype after prolonged cold exposure or pharmacological stimulation [ 63 ]. These three adipose tissue phenotypes have morphological differences and unique endocrine functions, which allows them to play important roles in human metabolism, especially in relation to obesity and its associated diseases, such as CVD. An example of a phenotypic difference within a single depot is the para-aortic fatty tissue, with thoracic para-aortic fatty tissue being morphologically similar to brown adipose tissue and being comprised of adipocytes with a multi-coloured appearance and round nucleus. Direct comparison of murine PVAT gene expression in the thoracic aortic and intercapsular white and brown adipose tissues revealed significant differences in the expression of only genes i. In contrast with thoracic aortic fatty tissue, abdominal aortic fatty tissue is more similar to white adipose tissue [ 64 ], especially in obese mice, where the abdominal aortic PVAT is similar to white adipose tissue i. In addition, mesenteric PVAT is characterized by adipocytes with large lipid drops and low levels of uncoupling protein-1 expression. Obesity can also be related to changing local fat depots, with excessive accumulation of subcutaneous fat being accompanied by an increase in the number of adipocytes and the absence of metabolic disorders. However, the accumulation of visceral fat leads to an increase in the size of adipocytes and increases their sensitivity to the effects of catecholamines, intense lipolysis, the development of insulin resistance, and adipokine and proinflammatory imbalance. In addition, visceral adipocytes unlike subcutaneous adipocytes are characterized by a high density of androgenic corticosteroid receptors, rich innervation, a wide capillary network, and a high metabolic activity. Thus, prostate tissue adipocytes predominantly exhibit adiponectin production, whereas SAT adipocytes predominantly synthesize leptin. Epicardial adipocytes have high proinflammatory activity, whereas most perivascular adipocytes do not synthesize TNF-alpha [ 65 ]. These differences may be related to the phenotypes of the different adipose tissues. For example, the unfavourable metabolic effects of VAT are facilitated by anatomical proximity to the portal vein, which passes through the abdominal fat and allows factors that are formed during FFA lipolysis to reach the liver. In hypertrophied adipocytes, the insulin-dependent glucose uptake is reduced due to deficiency of the GLUT4 receptors, which aggravates hyperglycaemia and insulin resistance. In addition, systematic circulation of FFA contributes to decreased glucose uptake and its utilization in muscle tissue, which strengthens peripheral insulin resistance. Excess FFA and insulin resistance, combined with visceral obesity, lead to disruption of lipid metabolism and the development of atherogenic dyslipidaemia. Thus, disruption of carbohydrate and lipid metabolism creates a vicious cycle, with FFA synthesized by visceral adipocytes serving as a key catalyst. Therefore, each local fat depot can be considered an independent endocrine organ that actively produces biologically active molecules, such as pro- and anti-inflammatory cytokines and adipokines, although the effects of each depot vary greatly. It is known that each local fat depot can be considered an independent endocrine organ that actively produces biologically active molecules, such as pro- and anti-inflammatory cytokines and adipokines. However, the effects of each depot vary greatly, with SAT adipocytes predominantly producing adiponectin and VAT adipocytes more actively synthesizing leptin. Epicardial adipocytes have a high pro-inflammatory activity, whereas most perivascular adipocytes do not synthesize TNF-alpha. These mechanistic differences may be attributed to the phenotype of each adipose tissue depot. For example, the properties of PVAT may be attributed to brown adipose tissue, including its cellular morphology and the expression of characteristic thermogenic genes. However, the phenotype of PVAT near other vessels is relatively heterogeneous, which may be attributed to the phylogenetic origins of PVAT and other adipose tissues. Thus, it remains unclear whether PVAT is a classic brown, beige, or white adipose tissue with changing characteristics, and similar phenotypic properties are manifested by paranephric fatty tissue. 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Perivascular adipose tissue alleviates inflammatory factors and stenosis in diabetic blood vessels. Methods and Results: This was a cross-sectional study of normal children and adolescents, age years, 68 male and 55 black. Dual energy x-ray absorptiometry was used to measure total and regional fat mass. The distribution of fat was calculated as the fat mass in the subscapular and waist region divided by fat mass in the hip and thigh region. The dependent variables were fasting lipid and lipoprotein concentrations, systolic and diastolic blood pressure BP , and left ventricular mass LVM measured by echocardiography. The distribution of fat entered the multiple regression models prior to any other measure of adiposity. Conclusion : These results demonstrate that the distribution of fat is a more important independent predictor of cardiovascular risk factors than percent body fat in children and adolescents. Greater deposition of central fat an android fat pattern is associated with less favorable lipid and lipoprotein concentrations, blood pressure and left ventricular mass. Division of Cardiology, Children's Hospital Medical Center, Cincinnati, OH, USA. Division of Cardiology, Cleveland Clinic Foundation, Cleveland, OH, USA. You can also search for this author in PubMed Google Scholar. Reprints and permissions. Daniels, S. et al. Pediatr Res 43 Suppl 4 , 90 Download citation. Issue Date : 01 April Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. |
| Rights and permissions | Treatment for cardiovadcular was also recorded. Gut health and leaky gut syndrome aim of Fat distribution and cardiovascular disease study Sports nutrition guidelines to determine the body fat distribution and cardiovascular distributioj risk factors in pre- and postmenopausal cardiovawcular women disgribution for weight, height and body mass index BMI. Dev Med Child Neurol. A need for better assessments. Article CAS PubMed Google Scholar Kanai H, Matsuzawa Y, Kotani K, Keno Y, Kobatake T, Nagai Y, et al. Article PubMed Central CAS PubMed Google Scholar Enomoto T, Ohashi K, Shibata R, Higuchi A, Maruyama S, Izumiya Y, et al. |
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