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Extreme Fat Burn: Thermogenic Weight Loss (psychic/morphic energy programmed) by Sapien MedicineThermogenesis and fat oxidation -
a Time course of changes in REE and RQ after Sham drink or DW in 27 young adults. b — d Frequency distribution of changes in REE and RQ after Sham drinking b and DW drinking c ; the red colour line being the normal curve. In d , the individual values are plotted for changes after DW drinking versus after Sham drinking; the dotted diagonal line being the line of identity, and the solid line being the regression line r values are not significant.
However, Sham drinking also led to a gradual and significant fall in RQ, albeit without the evident initial transient change. As shown in Figures 1b and c right-hand side , the frequency distribution of changes in RQ after DW is not different compared with that for Sham drinking, and furthermore there is no correlation between the changes in RQ after DW versus Sham drinking Figure 1d.
Analysis of the data for potential gender differences indicates no significant differences between men and women in their REE or RQ responses to DW or to Sham drink Supplementary Information, section A.
Although within each gender, there is a tendency for the increase in REE to be higher with DW than with Sham drink, these differences are small and not statistically significant, and within each drink type, men and women did not differ significantly in their changes in REE or RQ.
The main findings of this study investigating the acute metabolic effects of water per se , that is, in purified form as DW, can be summarized as follows:. RQ was consistently shown to fall after the DW drink, independently of gender, but it also diminished to a similar extent in response to Sham drinking.
The interindividual variability in REE and RQ response was not associated with body fatness, central adiposity or parameters of lean body mass. Although REE relative to baseline was significantly increased by 2.
Indeed, no significant difference can be demonstrated in REE after DW compared with REE after Sham drinking, both in men and women, suggesting that the ingestion of the water load per se does not lead to the stimulation of thermogenesis.
A possible explanation for the small increase in REE after DW, also found in response to the Sham drink, could reside in the psychobiological, and perhaps sensorial, aspects related to the act associated with drinking that is, without actually ingesting the water rather than the effect of the ingested water load per se.
The importance of Sham drinking in the interpretation of the reduction in RQ after the water drink is underscored in our study here. We found significant reductions in RQ with time after the water drink, but also after Sham drinking.
All these values are within or close to ±2 s. Consequently, the DW response cannot be attributed to effects of ingested water per se. Overall, the findings of large increases in REE after water drinking reported by Boschmann et al.
Data are for 20 experiments conducted in several laboratories see Table 1 for references , including the current study I for data presented in main text, and II for data presented in Supplementary Information, section B.
Individual values are represented as filled circles; otherwise the mean values are indicated as triangles. Water types are abbreviated as follows: TW, tap water; DW, distilled water; MW, mineral water. Unlabeled studies are those for which water type was not specified.
The grey zone represents the range of values within mean±2 s. of ΔREE after Sham drinking in young adults in our experiment.
Boschmann et al. By contrast, because respiratory chambers have a slower response time, and the data for REE and RQ are confounded by early activities within the chamber, they are therefore less suitable for acute measurements.
Unfortunately, they did not provide any data to support this contention. Water-induced thermogenesis in Boschmann et al.
Indeed, whether the presence of minerals in bottled water used in the studies of Kocelak et al. Our findings here, in a relatively large group of men and women that drinking pure water failed to induce more than marginal change in REE—in any of the participants—call for a re-evaluation of the rationale underlying the concept of water-induced thermogenesis, in particular:.
In fact, in Boschmann et al. Furthermore, if the hypothesis of water-induced thermogenesis is correct, then drinking cold water should stimulate further its thermogenic effect. Although Brown et al. Thus, most of the energy required for warming the water to body temperature is most likely met through diminished body heat loss, probably via peripheral vasoconstriction that occurs after water drinking.
The rationale for studies investigating water-induced thermogenesis derives from earlier findings that drinking half a litre of water increases SNS activity, as measured by enhanced plasma noradrenaline levels 4 and muscle sympathetic nerve activity. It should, however, be emphasized that there is considerable heterogeneity in sympathetic activation vis-à-vis physiological functions.
Indeed, infusion of noradrenaline in humans results in an increase in whole-body REE, but without detectable increase in oxygen consumption in forearm skeletal muscle. In fact, the observed increase in muscle sympathetic activity after water drinking may only be influencing the muscle vasculature rather than myocyte metabolism.
This contention is consistent with findings that the increase in SNS activity after water drinking is accompanied by peripheral vasoconstriction and diminished limb blood flow. Using the ventilated hood indirect calorimetry system, considered to be most appropriate approach to study acute changes in REE and RQ, our study comparing the ingestion of purified distilled water to Sham drinking suggests that water ingestion per se does not result in stimulation of thermogenesis or fat oxidation in healthy young men and women varying widely in adiposity.
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Circulating NEFA is directed toward TAG replenishment in brown adipocytes although a portion of NEFA contributes to thermogenesis 35 , These FAs are ligated to CoA groups before being converted to acyl-carnitine for mitochondrial import through carnitine palmitoyltransferase 1 CPT1 located in the outer mitochondrial membrane OMM.
Subsequent FA β-oxidation in the matrix produces acetyl-CoA, which then enters the TCA cycle as citrate after condensation with oxaloacetate OAA. FAO results in a larger increase in acetyl-CoA levels per molecule of nutrient than glucose-derived pyruvate oxidation i. Accordingly, FAO is more efficient in generating NADH and FADH 2 and FA has been viewed as the primary substrate for energy-demanding brown adipocyte mitochondria 1 , 6.
Moreover, it is interesting to note that FA is not only the energy substrate for thermogenesis but also activates the UCP1-mediated proton leak across the IMM 29 , Surprisingly, activated brown adipocytes also take up large amounts of glucose from the circulation while primarily utilizing FA to fuel thermogenesis 19 , 41 — Therefore, it has been suggested that, while oxidizing FA to fuel thermogenesis, brown adipocytes concurrently increase glycolysis and de novo FAS to replenish intracellular TAG pool in lipid droplets 15 — However, it is currently unclear how brown adipocytes concurrently perform FAO and FAS in the same cell because these processes are two mutually exclusive pathways in healthy cells.
More interestingly, recent studies have shown that cold-activated BAT in rodents and humans utilizes additional substrates such as branched-chain amino acids BCAA 50 , 51 , glutamate 44 , and succinate 52 to support thermogenesis.
Extracellular succinate contributes to thermogenic respiration in BAT by the succinate dehydrogenase SDH -mediated oxidation in the TCA cycle 52 , although its relative contribution to thermogenesis is unclear.
It is also possible that carbons from these additional substrates replenish TCA cycle intermediates that leave the cycle for biosynthetic pathways e. In most mammalian cells, mitochondrial FAO suppresses glycolysis, pyruvate oxidation, and de novo FAS The resulting decrease in acetyl-CoA reduces the production of pyruvate-derived citrate that exits the mitochondria to serve as the precursor for FAS.
Thus, FAO-dependent inhibition of PDH activity in the mitochondria is the primary mechanism preventing both pyruvate oxidation and de novo FAS from glucose. Additionally, FAO can inhibit glycolysis. A portion of excess citrate produced from FA-derived acetyl-CoA is exported to the cytosol, where it in turn inhibits glycolytic enzymes, such as phosphofructokinases PFK1, PFK2 and pyruvate kinase PK 20 , 55 — Conversely, when extracellular glucose increases, enhanced glycolysis provides more pyruvate to the mitochondria.
The conversion of pyruvate to acetyl-CoA by PDH and to OAA by pyruvate carboxylase PC increases citrate production in the mitochondria. Under high glucose, excess citrate is exported to the cytosol and hydrolyzed back to acetyl-CoA and OAA by ATP-citrate lyase ACLY.
Acetyl-CoA is then carboxylated to malonyl-CoA by two acetyl-CoA carboxylases, ACC1 and ACC2 Malonyl-CoA is the precursor of de novo synthesized FA.
Remarkably, malonyl-CoA produced by ACC2 allosterically inhibits CPT1 59 , 60 that controls the entry of long-chain fatty acids from the cytosol into mitochondria. By this mechanism, glucose-derived malonyl-CoA prevents the oxidation of newly synthesized and pre-existing FAs. Thus, malonyl-CoA is a key metabolite regulating the balance between FAS and FAO.
ACC1 is cytosolic and directs malonyl-CoA toward de novo FA synthesis catalyzed by fatty acid synthase FAS. In contrast, ACC2 is associated with the OMM and regulates FAO through malonyl-CoA-mediated CPT1 inhibition 59 — 61 , While lipogenic WAT predominantly expresses ACC1, BAT expresses similar amounts of ACC1 and ACC2 In addition, BAT expresses CPT1β, an isoform with high sensitivity to malonyl-CoA 65 — Despite the expression of ACC2 and CPT1β, BAT mitochondria have the highest CPT1 activity among the tissues expressing CPT1β 65 — High FAO in BAT is surprising in light of the inhibitory effect of malonyl-CoA produced by ACC2 on CPT1β-mediated FA transport.
It is unclear whether ACC2 activity or association to the mitochondria is negatively regulated by cold in brown adipocytes. It is interesting to note that concurrent FAO and FAS have also been observed in a subset of cancer cells 68 — Glycolytic colorectal cancer cells recruit FAO as an adaptive response to extracellular acidification associated with increased pyruvate to lactate conversion A selective decrease in the transcription of ACACB gene under acidosis was in part the mechanism permitting mitochondrial FAO.
However, it is unlikely that the selective decrease in ACACB gene expression provides a mechanism by which brown adipocytes concurrently perform FAO and FAS because BAT upregulates the expression of both ACACA and ACACB genes encoding ACC1 and ACC2, respectively, in response to cold As another example, a subset of highly proliferating B-cell lymphomas concurrently stimulates mitochondrial FAO while increasing glycolysis and FAS 69 ; however, the underlying mechanism remains unknown.
Single-cell and single-nucleus RNA sequencing of BAT has uncovered the existence of multiple brown adipocyte subpopulations with large variability in their transcriptomes and with different degrees of thermogenic capacities 71 — Compared with the high-thermogenic brown adipocytes, low-thermogenic brown adipocytes express lower levels of Ucp1 along with reduced mitochondrial respiration The co-existence of functionally different brown adipocytes within the BAT may in part explain how BAT performs FAO and FAS simultaneously.
Further studies are required to delineate the location, functional specialization, and substrate utilization of these brown adipocyte subpopulations and their ratios in response to environmental stimuli. In addition to heterogeneity of brown adipocytes, recent studies have demonstrated the presence of metabolically distinct populations of mitochondria within the same brown adipocyte: cytosolic mitochondria CM and peridroplet mitochondria PDM 74 — PDM are found to be anchored to the lipid droplets and have reduced motility and fusion-fission dynamics that segregate PDM from the rest of the mitochondrial population 79 , While CM preferentially oxidize FA for theromgenesis, PDM have a higher capacity for pyruvate oxidation and ATP synthesis 74 Figure 2.
In line with increased oxidative phosphorylation, PDM is enriched with ATP synthase compared to CM 74 although UCP1 levels are comparable in PDM and CM 74 , More interestingly, an increase in PDM is associated with lipid droplet expansion in brown adipocytes Given that coupled respiration is dependent on ADP availability, excess citrate produced from pyruvate-derived acetyl-CoA in the PDM may exit the mitochondria and be converted to malonyl-CoA by ACC1 and ACC2, thus contributing to de novo FAS for TAG synthesis and concurrently preventing FA entry into these specific subpopulations of mitochondria Figure 2.
On the contrary, in CM preferentially oxidizing FA 74 , FA-derived acetyl-CoA could inhibit PDH activity, resulting in a decrease in pyruvate-derived citrate production and subsequent malonyl-CoA accumulation in close vicinity of CM Figure 2.
It is unclear whether there is a difference in ACC2 levels between PDM and CM. CM could maximize UCP1-mediated thermogenesis by producing high levels of NADH and FADH 2 from FAO. The resulting rapid oxidation of FA-derived citrate through the TCA cycle may prevent citrate export to the cytosol for inhibition of glycolytic enzymes.
Figure 2 The co-existence of two functionally different mitochondria within the brown adipocyte. A scheme of two types of mitochondria identified in the brown adipocyte: cytosolic mitochondria CM and peridroplet mitochondria PDM 74 — PDM are anchored to the lipid droplets and segregated from the pool of CM.
CM preferentially oxidize FA and are more thermogenic compared to PDM. FA-derived citrate would be rapidly oxidized through the TCA cycle to support UCP1-mediated thermogenesis. On the contrary, PDM have a higher capacity for pyruvate oxidation and ATP synthesis compared to CM. Given that coupled respiration is dependent on ADP availability, excess citrate would escape from the mitochondria and be converted to malonyl-CoA by ACC1 and ACC2, thus contributing to de novo lipogenesis and simultaneously preventing CPT1β-mediated FA entry into PDM.
The co-existence of two functionally different mitochondria within the brown adipocyte may in part explain the concurrence of glycolysis, FA synthesis, and FA oxidation in brown adipocytes. FA, fatty acids; ETC, electron transport chain; CPT, carnitine palmitoyltransferase; UCP1, uncoupled protein 1; TCA, the tricarboxylic acid cycle; OAA, oxaloacetate; MPC, mitochondrial pyruvate carrier; PDH, pyruvate dehydrogenase; PC, pyruvate carboxylase; ACLY, ATP-citrate lyase; ACC, acetyl-CoA carboxylases; FAS, fatty acid synthase; TAG, triacylglycerol.
In contrast to the lipogenic role of PDM in brown adipocytes, several studies reported conflicting results that PDM promotes the oxidation of FA released from lipid droplets 77 , This discrepancy may imply that the role of PDM is differently regulated by the cell type, nutritional status, or cellular stress.
Proteome profiling of PDM and CM in BAT has identified a subset of mitochondrial proteins differentially expressed between PDM and CM although their impact on the functional difference has not been explored Additional studies are required to quantitatively characterize PDM and CM mitochondrial proteins e.
Brown adipocytes have two unique features: 1 UCP1-mediated dissipation of the PMF, which provides a mechanism for maximal substrate oxidation in the mitochondria and 2 concurrence of glycolysis, de novo FAS, and FAO.
Upon activation, brown adipocytes increase glycolysis and de novo FAS to replenish intracellular TAG pools that are depleted due to increased lipolysis and FAO. The co-existence of FA-oxidizing and lipogenic mitochondria within the brown adipocyte in addition to heterogeneity of brown adipocytes may in part explain the unique capacity of brown adipocytes to be involved simultaneously in FAO and FAS.
The author confirms being the sole contributor of this work and has approved it for publication. The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Cannon B, Nedergaard J. Brown adipose tissue: Function and physiological significance.
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Thermogenesis and fat oxidation PDF. This study was oxidaation by Grant-in-Aid Thermogeneiss Scientific Research from the Ministry of Education, Thermobenesis, Sports, Oxiidation and Technology of Japan, 17K to Oxidattion Yuko, and 16K, 18K to Masayuki Saito. Skip Navigation Skip to contents Search Home Current Cancer prevention for men issue Cancer prevention for men print Browse All issues Article Thermgoenesis category Article by topic Oxidahion by Category Best paper of the Meal planning Most view Most cited Thermogenesis and fat oxidation Essential fatty acids Diabetes Metab Oixdation Search Oxjdation index Collections Guidelines in DMJ Fact sheets in DMJ COVID in DMJ For contributors For Authors Instructions to authors Article processing charge e-submission For Reviewers Instructions for reviewers How to become a reviewer Best reviewers For Readers Readership Subscription Permission guidelines About Aims and scope About the journal Editorial board Management team Best practice Metrics Contact us Editorial policy Research and publication ethics Peer review policy Copyright and open access policy Article sharing author self-archiving policy Archiving policy Data sharing policy Preprint policy Advertising policy E-Submission. mobile menu button. Author information Article notes Copyright and License information 1 Faculty of Veterinary Medicine, Hokkaido University, Sapporo, Japan 2 Department of Nutrition, Tenshi College, Sapporo, Japan Corresponding author: Masayuki Saito Faculty of Veterinary Medicine, Hokkaido University, SapporoJapan E-mail: saito vetmed. ABSTRACT Brown adipose tissue BAT is a specialized tissue for nonshivering thermogenesis to dissipate energy as heat. Thermogenesis and fat oxidation adipocytes Thermogeesis a specialized fat cell that dissipates nutrient-derived chemical energy in the Thermogenesus of heat, instead of ATP synthesis. This unique feature provides Oxidatoin marked capacity for brown adipocyte mitochondria to oxidize oidation independent of Body composition and energy expenditure Cancer prevention for men. Upon cold exposure, brown adipocytes preferentially oxidize free fatty acids FFA liberated oxivation triacylglycerol Thermogenesis and fat oxidation in lipid droplets to support thermogenesis. In addition, brown adipocytes take up large amounts of circulating glucose, concurrently increasing glycolysis and de novo FA synthesis from glucose. Given that FA oxidation and glucose-derived FA synthesis are two antagonistic mitochondrial processes in the same cell, it has long been questioned how brown adipocytes run FA oxidation and FA synthesis simultaneously. In this review, I summarize mechanisms regulating mitochondrial substrate selection and describe recent findings of two distinct populations of brown adipocyte mitochondria with different substrate preferences. I further discuss how these mechanisms may permit a concurrent increase in glycolysis, FA synthesis, and FA oxidation in brown adipocytes.
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