Hyperglycemia and fertility -
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Investigation of the effect of body mass index BMI on semen parameters and male reproductive system hormones. Ghasemi H, Karimi J, Goodarzi MT, Khodadadi I, Tavilani H, Moridi H, Kheiripour N.
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The combined effect of obesity and aging on human sperm DNA methylation signatures: inclusion of BMI in the paternal germ line age prediction model. Sci Rep. Pini T, Parks J, Russ J, Dzieciatkowska M, Hansen KC, Schoolcraft WB, Katz-Jaffe M. Obesity significantly alters the human sperm proteome, with potential implications for fertility.
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Urol Sci. Taha EA, Algahny Algahlan HA, Zidan M, Abdelhafez A, Farag FF. Scrotal ultrasonographic findings in obese infertile patients and their correlations to semen and hormonal profile. Turkish J Urol.
Ferigolo PC, Ribeiro de Andrade MB, Camargo M, Carvalho VM, Cardozo KHM, Bertolla RP, Fraietta R. Sperm functional aspects and enriched proteomic pathways of seminal plasma of adult men with obesity.
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A large population study. Wang EY, Huang Y, Du QY, Yao GD, Sun YP. Body mass index effects sperm quality: a retrospective study in Northern China. Luque EM, Tissera A, Gaggino MP, Molina RI, Mangeaud A, Vincenti LM, Beltramone F, Larcher JS, Estofán D, Cuneo M, et al. Body mass index and human sperm quality: neither one extreme nor the other.
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J Androl. Existing cases of diabetic retinopathy become more pronounced during pregnancy, usually in the final trimester, and require treatment. Renal function should also be examined. It is also crucial that the blood sugar levels are optimally managed. As with all women who wish to get pregnant, specialist associations recommend beginning with iodine and folic acid tablets before the pregnancy.
Beginning at least 4 weeks before pregnancy and continuing until the end of the 12th week of pregnancy, women should take between 0. At least milligrams of an iodine prophylaxis supplement should be taken.
Information on iodine-rich food and the use of iodized salt is recommended. The aim is to ensure the fetus receives enough iodine and to prevent thyroid-related complications.
In cases of unwanted pregnancy, women with diabetes should seek medical advice as soon as possible. It may be necessary to adjust diabetes therapy before pregnancy. For women with type 1 diabetes , this may mean that their doctor recommends switching to another type of insulin preparation.
For women with type 2 diabetes , medical specialists recommend switching to insulin therapy. As with all types of medication, care should be taken during pregnancy.
For many types of blood sugar-reducing medications , there is little data available on their safety for the unborn child. For this reason, doctors recommend switching to insulin therapy human insulin before a planned pregnancy.
Intensified insulin therapy or an insulin pump are used. In some cases, it is possible to get blood sugar levels under control through lifestyle changes, sufficient exercise and a healthy diet. Finding the correct insulin dosage is not always easy.
On top of this, any change in treatment can cause often uncertainty. For this reason, women with type 2 diabetes should take part in a course to learn how to inject and measure blood sugar levels correctly. There they will learn to use an insulin pen or insulin pump.
The costs for the course are usually covered by the health insurance provider. Find out more about insulin therapy here! It is recommended that pregnant women measure their blood sugar levels 6 times per day 1 hour before each meal, and 1 hour after.
A safe and reliable blood sugar measurement device should be used for blood sugar self-testing. Blood sugar levels and insulin requirements change during pregnancy up until delivery due to the pregnancy hormones.
During the 1st trimester, the amount of insulin required falls. During this period, the expectant mother must inject less insulin to prevent low blood sugar levels. The insulin requirements increase rapidly during the 2nd trimester and then dramatically fall again after giving birth. During the 1st trimester, there is an increased risk of low blood sugar hypoglycemia , especially during the night.
To help estimate the risk of nocturnal low blood sugar, blood sugar levels can be tested at around 11 pm. The diabetes specialist responsible for treatment must carefully adjust the insulin dosage.
Pregnant women should definitely inform those close to them and their partner about what to do in the event of severely low blood sugar levels.
Ketoacidosis acid buildup in the blood caused by lack of insulin associated with pregnancy diabetes is an emergency situation. Expectant mothers discuss with their diabetes specialist at what blood sugar level they should begin testing acetone levels in the urine.
To ensure good management of type 1 or type 2 diabetes during pregnancy, the patient should attend the following check-ups, among others:. If the blood sugar levels are too high throughout pregnancy, the child can become too large and too heavy birth weight exceeding grams.
This can lead to complications during birth or cesarean section. Diabetes-related complications, e. During the later stages of pregnancy, expectant mothers can develop high blood pressure. In this case, self-testing of blood pressure can be carried out on a daily basis.
Pregnant women with diabetes are more likely to develop infections of the genital and urinary organs, which can lead to premature birth. For this reason, regular testing is recommended.
Preeclampsia, also known as gestosis or pregnancy poisoning, is especially serious. It is characterized by high blood pressure and increased excretion of protein via the urine proteinuria. Preeclampsia, the most severe form of gestosis, is a very serious emergency situation that requires immediate hospital treatment.
Women with type 1 diabetes in particular can develop low blood sugar levels during the 1st trimester, especially at night. Therefore, it may be necessary to temporarily change or adjust their course of treatment.
Later in pregnancy, the blood sugar levels become more stable and the risk drops. The internal organs of the fetus develop during the 1st trimester of pregnancy. If the blood sugar levels are not optimally regulated before and during pregnancy, this can result in malformation of the heart, nervous system, and lungs in particular.
Miscarriage and premature birth are also possible. The risk of premature birth birth before the end of the 37th week of pregnancy is on average 5 times higher for expectant mothers with diabetes. These risks can be significantly reduced thanks to targeted consultation, good metabolic management, and blood sugar self-testing.
Other typical complications include low blood sugar, jaundice hyperbilirubinemia , or respiratory disorders.
Around 5 percent of children from mothers or fathers with type 1 diabetes will also develop diabetes mellitus, because the disease is partially genetically determined.
Diabetes mellitus and sperm parameters. J Androl — High levels of lipid peroxidation in semen of diabetic patients. Andrologia 44 Suppl 1 — The influence of type 1 diabetes mellitus on spermatogenic gene expression.
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Reprod Biomed Online —9. Lestienne P, Reynier P, Chretien MF, Penisson-Besnier I, Malthièry Y, Rohmer V. Oligoasthenospermia associated with multiple mitochondrial DNA rearrangements. Mol Hum Reprod —4. Silvestroni L, Modesti A, Sartori C. Insulin-sperm interaction: effects on plasma membrane and binding to acrosome.
Arch Androl — Cameron DF, Murray FT, Drylie DD. Interstitial compartment pathology and spermatogenic disruption in testes from impotent diabetic men. Anat Rec — Chan JL, Mantzoros CS. Leptin and the hypothalamic-pituitary regulation of the gonadotropin-gonadal axis.
Pituitary — Pitteloud N, Hardin M, Dwyer AA, Valassi E, Yialamas M, Elahi D, et al. Increasing insulin resistance is associated with a decrease in Leydig cell testosterone secretion in men.
J Clin Endocrinol Metab — Amaral S, Oliveira PJ, Ramalho-Santos J. Diabetes and the impairment of reproductive function: possiblerole of mitochondria and reactive oxygen species. Curr Diabetes Rev — Mallidis C, Agbaje IM, Rogers DA, Glenn JV, Pringle R, Atkinson AB, et al. Advanced glycation end products accumulate in the reproductive tract of men with diabetes.
Condorelli RA, Calogero AE, Vicari E, Duca Y, Favilla V, Morgia G, et al. J Endocrinol Invest —4. Patterson JE, Andriole VT. Bacterial urinary tract infections in diabetes. Infect Dis Clin North Am — Guest CB, Park MJ, Johnson DR, Freund GG. The implication of proinflammatory cytokines in type 2 diabetes.
Front Biosci — La Vignera S, Di Mauro M, Condorelli R, La Rosa S, Vicari E. Clin Ter 5 —6. Google Scholar. La Vignera S, Calogero AE, Condorelli R, Lanzafame F, Giammusso B, Vicari E.
Andrological characterization of the patient with diabetes mellitus. Minerva Endocrinol 34 1 :1—9. PubMed Abstract Google Scholar. American Diabetes Association. Standards of medical care in diabetes — Diabetes Care S11— Zegers-Hochschild F, Adamson GD, Dyer S, Racowsky C, de Mouzon J, Sokol R, et al.
The international glossary on infertility and fertility care. Hum Reprod — World Health Organization. WHO Laboratory Manual for the Examination and Processing of Human Semen.
Cambridge, UK: Cambridge University Press La Vignera S, Condorelli RA, Vicari E, Salmeri M, Morgia G, Favilla V, et al. Microbiological investigation in male infertility: a practical overview.
J Med Microbiol — Barbonetti A, Vassallo MR, Di Rosa A, Leombruni Y, Felzani G, Gandini L, et al. Involvement of mitochondrial dysfunction in the adverse effect exerted by seminal plasma from men with spinal cord injury on sperm motility. Andrology — Niven MJ, Hitman GA, Badenoch DF.
A study of spermatozoal motility in type 1 diabetes mellitus. Diabet Med —4. Ali ST, Shaikh RN, Siddiqi NA, Siddiqi PQ. Padrón RS, Dambay A, Suarez R, Màs J.
Semen analyses in adolescent diabetic patients. Acta Diabetol Lat — Amaral A, Lourenço B, Marques M, Ramalho-Santos J. Mithocondria functionality and sperm quality. Reproduction — Altered ultrastructure of mithocondrial membranes is strongly associated with unexplained asthenozoospermia.
Fertil Steril —6. Seshadri S, Flanagan B, Vince G, Lewis-Jones DJ. Detection of subpopulations of leucocytes in different subgroups of semen sample qualities. Andrologia — Witkin SS.
Mechanisms of active suppression of the immune response to spermatozoa. Am J Reprod Immunol Microbiol —4. El-Badawi A, Schenk EA.
The distribution of cholinergic and adrenergic nerves in the mammalian epididymis: a comparative histochemical study. Am J Anat — Kempinas WD, Suarez JD, Roberts NL, Strader L, Ferrell J, Goldman JM, et al. Rat epididymal sperm quantity, quality, and transit time after guanethidine-induced sympathectomy.
Biol Reprod —6. Keywords: type 1 diabetes mellitus, type 2 diabetes mellitus, infertility, conventional sperm parameters, biofunctional sperm parameters, sperm function.
Citation: Condorelli RA, La Vignera S, Mongioì LM, Alamo A and Calogero AE Diabetes Mellitus and Infertility: Different Pathophysiological Effects in Type 1 and Type 2 on Sperm Function.
doi: Received: 01 February ; Accepted: 08 May ; Published: 25 May Copyright: © Condorelli, La Vignera, Mongioì, Alamo and Calogero. This is an open-access article distributed under the terms of the Creative Commons Attribution License CC BY.
The use, distribution or reproduction in other forums is permitted, provided the original author s and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Metrics details. The present study performed two distinct meta-analyses Hyperglycemia and fertility common outcomes sperm parameters ; one feryility performed in obese individuals ferrtility non-obese controls and Hypoglycemia and hypothyroidism other feftility diabetic individuals and non-diabetic controls. PubMed, Embase, The Cochrane library, Web of Science, Scopus databases were searched to collect clinical studies related to the effects of obesity and diabetes on male sperm from inception to on 1st February Statistical meta-analyses were performed using the RevMan 5. Stata16 software was used to detect publication bias. Anthocyanins and heart health apologize for the fertiliy, but your feritlity is currently Hypetglycemia supported by this website. Please try Hyperglycemia and fertility Hyperrglycemia, or install the latest version of Hyperglycemia and fertility fertilitj browser below:. Diabetes impacts Enhancing cholesterol profile than 30 million Americans with almost a quarter unaware that they have the disease. Diabetes has a lifelong impact on the health of those who have it, causing a variety of health problems such as blindness, nerve damage, and kidney disease. But it also impacts an aspect of your health that is rarely discussed — your reproductive health. For national Diabetes Awareness Month, the fertility experts of UNC Fertility are here to discuss the impact that diabetes can have on both male and female fertility.
Hyperglycemia and fertility -
DM2 patients were not subdivided according to duration of illness to avoid bias related due to age-related disease. This is because DM2 occurs temporally after DM1 and all patients enrolled were in childbearing age.
DM2 patients reported a previous nonalcoholic steatohepatitis returned after weight loss. All enrolled subjects did not smoke, drink alcohol, and did not use drugs. All methods were performed in accordance with the relevant guidelines and regulations. All participants were asked for and provided their informed consent.
Oxidative stress evaluation in the seminal fluid was executed by measuring the degree of mitochondrial superoxide and the degree of LP. Seminal analysis of each sample was replicated as reported by the WHO guidelines.
Semen samples were collected by masturbation into a sterile container after 2—7 days of sexual abstinence and were transported to the laboratory within 30 min after ejaculation. Each sample was evaluated for seminal volume, pH, viscosity, sperm count, progressive motility, morphology, and round cell concentration spermatids and leukocytes according to the WHO criteria The debris was gated out, by drawing a region on forward vs.
side scatter dot plot enclosing the population of cells of interest. Computed compensation was made before performing all the analyses. The damage of MMP is an early event of the apoptosis and it is reversible. JC-1 is able to penetrate selectively in mitochondria and it exists in monomeric form, emitting at nm; following excitation at nm and in relation to the membrane potential, JC-1 is able to form aggregates emitting at nm.
The fluorescence changes reversibly from green to orange as soon as the mitochondrial membrane becomes more polarized. Therefore, it is possible to distinguish two cell populations: cells with damaged MMP where JC-1 remains in the cytoplasm in a monomeric form, giving a green fluorescence and cells with normal MMP with a double fluorescence where JC-1 in addition to emitting green in the cytosol is also in the mitochondrial membrane in form of aggregates emitting in an orange fluorescence.
At the end of the incubation period, the cells were washed in phosphate buffered saline PBS and analyzed by the detectors FL1 and FL3. The evaluation of chromatin integrity was performed after permeabilization of the cell membrane, to allow the access of the fluorophore within the nucleus.
An aliquot of 1 × 10 6 spermatozoa was incubated with LPR DNA-Prep Reagent containing 0. Flow cytometric analysis was performed after 30 min, using FL3 detector. The externalization of phosphatidylserine PS on the outer cell surface is an early signal of apoptosis. The assessment of PS externalization was performed using annexin V, protein that binds selectively to PS in presence of calcium ions, FITC-labeled.
During apoptosis, the cells exhibiting the PS even before the loss of semipermeability. Therefore, marking simultaneously the cells with annexin V and PI, we could distinguish: alive with intact cytoplasmic membrane , apoptotic, or necrotic cells.
An aliquot containing 0. After incubation, the sample was analyzed immediately by the detectors FL1 FITC and FL3 PI. The different pattern of staining allowed to identify the different cell populations: FITC negative and PI negative indicate viable cells, FITC positive and PI negative indicate cells in early apoptosis with cytoplasmic membrane still intact, and FITC positive and PI positive indicate cells in late apoptosis.
The evaluation of DNA fragmentation was performed by the TUNEL method. This uses the Terminal deoxynucleotidyl Transferase TdT , an enzyme that polymerizes, at the level of DNA breaks, modified nucleotides conjugated to a fluorochrome.
The TUNEL assay was performed by using a commercially available kit DBA s. To obtain a negative control, TdT was omitted from the reaction mixture; the positive control was obtained pretreating spermatozoa about 0. The debris was gated out as described above. The reading by threshold-setting method was performed by flow cytometry using the FL1 detector.
This displacement of the emission is shown by the flow cytometer which provides an estimate of the degree of peroxidation. LP was evaluated in two different sperm aliquots of the same patient: the first consisting of spermatozoa separated by swim-up and the second obtained by centrifugation of the seminal fluid raw semen.
About 2 × 10 6 of spermatozoa were incubated with 5 mM of the probe for 30 min in a final volume of 1 ml. After washing with PBS, flow cytometric analysis was conducted using the FL1 and FL2 detectors. Mitochondrial superoxide levels were detected by the MitoSOX red mitochondrial superoxide indicator Invitrogen, Thermo Fisher Scientific, Eugene, OR, USA This probe, once penetrated into the mitochondria, is quickly oxidized by superoxide anion not from other free radicals and as a result of this process, the probe becomes highly fluorescent with signal detection.
About 1 × 10 6 of spermatozoa were incubated with 5 µM of the probe for 10 min in a final volume of 1 ml and at a temperature of 37°C. After washing with PBS, flow cytometric analysis was conducted using FL1 detectors.
Specifically, after liquefaction, three aliquots of µl of seminal fluid underwent to three washing cycles with PBS. After elimination of the supernatant, the pellet was resuspended in 1 ml of PBS.
All patients underwent didymo-epididymal ultrasound evaluation using a linear 7. Ultrasound evaluation of the testicular volume and epididymal diameters was performed, before and after ejaculation, by the same clinician SLV. The ultrasound parameters evaluated were epididymal caput CEAE and tail TEAE after ejaculation, testicular volume VT , cranial CEBE , and caudal TEBE diameter before ejaculation.
The operator repeated twice the measurement of these parameters are expressed as mean on the final report. Blood sampling was performed at 8.
Determination of LH, FSH, and TT serum levels was performed by electrochemiluminescence immunoassay with Cobas equipment. The results are expressed as mean ± SEM throughout the study. SPSS Statistical significance was accepted when the p value was lower than 0.
The anthropometric parameters of the patients enrolled in this study are shown in Table 1. DM patients showed no statistically significant differences in age, BMI, and waist circumference compared to controls Table 1.
Table 1. Anthropometric parameters of patients with type 1 diabetes mellitus DM1 , type 2 diabetes mellitus DM2 , and the control CTL group. Conventional sperm parameters were significantly different in the three groups of patients Figure 1. Patients with DM1 or DM2 showed a statistically significant decrease in sperm concentration as compared to controls and DM2 patients had a slightly lower sperm concentration than DM1 patients.
Figure 1. Conventional sperm parameters in patients with type 1 diabetes mellitus DM1 , type 2 diabetes mellitus DM2 , and the control CTL group.
The results are expressed as mean ± SEM. Figure 2. Dot plot related to flow cytometric evaluation of mitochondrial membrane potential in a control, in a patient with type 1 diabetes mellitus DM1 , and in a patient with type 2 diabetes mellitus DM2 A.
Dot plot related to DNA fragmentation, with negative control NC , for threshold-setting method, in a control, in a patient with DM1, and in a patient with DM2 C. Figure 3. Biofunctional sperm parameters in patients with type 1 diabetes mellitus DM1 , type 2 diabetes mellitus DM2 , and control CTL group.
The other conventional sperm parameters did not appear significantly different. The other biofunctional sperm parameters did not vary significantly Table 2.
HbA1c levels did not correlate with any of the examined parameters data not shown. Table 2. Conventional and biofunctional sperm parameters in patients with type 1 diabetes mellitus DM1 according to the duration of the disease.
Figure 4. Leukocyte subpopulations in the seminal fluid of patients with type 2 diabetes mellitus DM2 and controls CTL. Data are expressed as mean ± SEM. Figure 5. Lipid peroxidation LP and mitochondrial superoxide concentrations type 1 diabetes mellitus DM1 , type 2 diabetes mellitus DM2 , and controls CTL in seminal fluid.
Table 3. Didymo-epididymal parameters in patients with type 1 diabetes mellitus DM1 according to the duration of the disease. FSH was not reveal significantly different in DM patients compared to controls Table 4. When patients with DM1 were classified according to the duration of the disease, no statistically significant difference was observed among three groups data not shown.
Table 4. Hormone concentrations of patients with type 1 diabetes mellitus DM1 , type 2 diabetes mellitus DM2 , and the control CTL group. The results of this study showed that diabetic patients in childbearing age have alterations of conventional sperm parameters compared to non-diabetic controls.
Of particular, the main alterations concern sperm concentration, progressive motility, and normal forms. Patients with DM1 showed a progressive motility that significantly deteriorated alongside the duration of the disease. Previous studies did not show significant variations of this parameter and no correlation with age, disease duration, or HbA1c levels 8 , By contrast, other studies confirm our data showing a decrease in sperm progressive motility in patients with DM1 and DM2 28 and in 32 DM1 teenage patients Mitochondrial membrane potential is the main parameter that better reflects mitochondrial function, which regulates sperm motility.
An association between decreased sperm progressive motility and an increase in the percentage of spermatozoa with low MMP has been shown in both groups of diabetic patients compared to controls. Other studies have shown that mitochondrial ultrastructural alterations are associated with a decreased sperm motility 30 , In patients with DM1, the alteration of the mitochondrial function became evident in patients with a disease duration ranging between 5 and 10 years, whereas the alterations of sperm progressive motility became significant in patients with a disease duration greater than 10 years.
Therefore, mitochondrial alteration seems to anticipate the subsequent and physiological decrease in sperm motility. Sperm volume was lower in patients with DM2 although the difference did not reach the statistical significance, unlike to previously published data This discrepancy may relate to the fact that patients with DM2 enrolled by Ali and colleagues 28 had lower TT values than the control group.
In addition, patients with DM2 enrolled in the present study were younger, in childbearing age and not yet entirely affected by the age-related androgenic decline compared to those described in the literature.
These DM2 patients enrolled had normal TT levels but higher values of LH compared to controls to indicate an initial testicular alteration. So, this slight reduction of the sperm volume may, however, represent the beginning of a process that could worsen at a later age.
Instead, DM1 patients showed lower seminal fluid volume in the presence of normal blood circulating concentrations of androgens. The patients of our study have bigger epididymal head and tail diameters after ejaculation compared to controls, suggesting an alteration in the epididymal contractile function.
This phenomenon, indicative of a dysfunctional epididymal voiding capability, may be the cause of the decreased seminal fluid volume observed in these patients. Leukocytes present in the rete testis, vas deferens, and human ejaculate are predominantly T-suppressor lymphocytes The role of lymphocytes in the seminal fluid is not only antimicrobial but also to remove apoptotic or immature germ cells.
The presence of these lymphocytes could improve seminal quality because T-suppressor lymphocyte removal action would avoid the activation of T-helper lymphocytes against antigen-presenting cells decreasing the production of antisperm antibodies and their possible sperm damage Therefore, this could explain the increased percentage of T-suppressor lymphocytes in DM2 patients, where there is a greater number of apoptotic cells, while that of T-helper is decreased because of the absence of microbial agent and antigen-presenting cells.
With regards to oxidative stress indices, the mitochondrial superoxide anion concentration was found to be higher in DM2 than in DM1 patients.
Indeed, LP increases only in DM2 patients, especially in relation to the higher concentration of seminal fluid leukocytes of this group of patients. In DM2 patients, the increase of LP and mitochondrial superoxide anion may decrease MMP and consequently be responsible for a greater sperm motility decline than in DM1.
Recently, it has been shown that the epididymis is a potential target of the oxidative stress in diabetic patients. Immunohistochemical analysis has shown the presence of AGE receptors in this organ In addition, malonildialdehyde levels, the final product of LP, are higher in DM2 patients compared to controls 5 , 6.
These data are relevant to understand the physiopathological and clinical aspects that can address a more targeted and specific therapeutic approach.
In addition, a greater percentage of DM2 patients are less vital, in late apoptosis and with fragmentation of sperm DNA. These data, associated with an increased number of leukocytes in the seminal fluid, with an increased LP and levels of mitochondrial superoxide, indicate that oxidative stress is the leading cause of impaired sperm quality of DM2 patients.
Finally, the didymo-epididymal ultrasound evaluation revealed a lack of physiological contraction of the cranial and caudal portion of the epididymis after ejaculation in DM1 patients.
Conventionally, the ultrasound epididymal thickness decreases by approximately 3 mm after ejaculation, as found in DM1 patients with a duration of illness of less than 10 years.
Epididymal cranial and caudal tracts are characterized by a spontaneous peristalsis that can also carry immotile spermatozoa The caudal portion of the epididymis has a rich adrenergic innervation, which is activated during ejaculation.
Adrenergic denervation does not eliminate epididymal contractility This suggests that the contractility is mediated by a neuronal mechanism and other hormonal oxytocin and endothelin 1 and non-hormonal factors, which can alter the contractile function of the epididymis.
Type 1 diabetes mellitus patients have low ejaculate volume due to a lack of physiological epididymal contraction associated with mitochondrial damage that anticipates the subsequent decline of sperm progressive motility.
These findings are associated with an increased oxidative stress that can also alter other conventional sperm parameters, although to a lower extent than in DM2 patients. Type 2 diabetes mellitus patients, instead, seem to be characterized by an amicrobial inflammatory condition and increased concentration of seminal fluid leukocytes, which raises oxidative stress indices damaging conventional sperm parameters, sperm DNA, and vitality.
Since diabetic disease affects male fertility, the prevention of DM2 and the follow-up of seminal parameters in DM1 should be recommended in patients in childbearing age. RC is the principal investigator of this study. AC is the coordinator of all phases of this study. Other authors SV, LM, and AA were involved in methodological and statistical aspects.
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Hamilton BE, Ventura SJ. Fertility and abortion rates in the United States, — Int J Androl — CrossRef Full Text Google Scholar.
Lutz W. PubMed Abstract CrossRef Full Text Google Scholar. Silink M. Childhood diabetes: a global perspective. Horm Res —5. Lascar N, Brown J, Pattison H, Barnett AH, Bailey CJ, Bellary S. Type 2 diabetes in adolescents and young adults.
Lancet Diabetes Endocrinol — Diabetes mellitus and sperm parameters. Elevated cortisol can also cause hormonal disruptions for both men and women. Finding ways to de-stress will keep cortisol levels low, increasing the chances of pregnancy. Diabetes is entirely manageable, especially if caught early.
Medications and lifestyle factors play a major role in the diabetic effect on the body. If blood glucose levels fall too low or go too high, the results can completely disrupt everyday life. Diabetes increases the risk of having a stroke, glaucoma, high blood pressure, kidney failure, nerve damage, and foot problems.
Women with diabetes before pregnancy will need to be watched closely. Pregnancy will affect blood sugar levels, and medication will most likely need to be adjusted. High blood glucose within the first trimester can cause birth defects.
Children born to diabetic mothers often have a much higher birth weight due to the excess sugar passed through the placenta and are often delivered via cesarean.
The risk of a blood sugar crash right after birth is high, and many of the babies are monitored for several hours after birth. The child of a diabetic mother is also more likely to develop type 1 or type 2 diabetes later in life.
Women may also develop diabetes during pregnancy, known as gestational diabetes. Preeclampsia is a risk to all diabetic mothers. Uncontrolled blood sugar levels can lead to infertility problems among women and men. The leading causes of diabetic-related infertility in women can be attributed to polycystic ovary syndrome PCOS , irregular menstruation, and premature menopause.
For men, the leading causes are erectile dysfunction, low sperm count or poor sperm quality, and low testosterone. Diabetes can pose extra complications on fertility, but the symptoms are manageable. Changes in diet, daily exercise, and managing stress can help increase the chances of a pregnancy.
Speak with a fertility specialist to learn more about the connection between fertility and diabetes. Getting Pregnant With Diabetes Controlling blood sugar levels is a major part of diabetic management. Eat smart Improving diabetes starts with controlling blood sugar levels.
Stay active Maintaining a healthy weight is a large part of diabetic management. Manage stress Cortisol produces excess glucose.
Hyperglycsmia blood sugar Anthocyanins and heart health is a major part of Ane management. Pregnancy and the fertilith journey can Herbal pick-me-up tonic additional complications on the process. Lifestyle factors fertiliyy Anthocyanins and heart health diet and exercise can help with weight management and improve fertility. Plenty of children are born each year to diabetic parents. When the mother of the child has diabetes, the risks are higher but are still manageable. In addition to staying on top of insulin levels and medications, below are 3 tips for improving fertility with diabetes.
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