Insulin Resistance In Females Research Articles

Efficacy of Human Recombinant Growth Hormone in Females of a Non-Obese Hyperglycemic Mouse Model after Birth with Low Birth Weight.

We examined whether the administration of growth hormone (GH) improves insulin resistance in females of a non-obese hyperglycemic mouse model after birth with low birth weight (LBW), given that GH is known to increase muscle mass. The intrauterine Ischemia group underwent uterine artery occlusion for 15 min on day 16.5 of gestation. At 4 weeks of age, female mice in the Ischemia group were divided into the GH-treated (Ischemia-GH) and non-GH-treated (Ischemia) groups. At 8 weeks of age, the glucose metabolism, muscle pathology, and metabolome of liver were assessed. The insulin resistance index improved in the Ischemia-GH group compared with the Ischemia group (p = 0.034). The percentage of type 1 muscle fibers was higher in the Ischemia-GH group than the Ischemia group (p < 0.001); the muscle fiber type was altered by GH. In the liver, oxidative stress factors were reduced, and ATP production was increased in the Ischemia-GH group compared to the Ischemia group (p = 0.014), indicating the improved mitochondrial function of liver. GH administration is effective in improving insulin resistance by increasing the content of type 1 muscle fibers and improving mitochondrial function of liver in our non-obese hyperglycemic mouse model after birth with LBW.

Effect of whole-body vibration on insulin resistance in females with polycystic ovarian syndrome: A randomized controlled trial

Effect of whole-body vibration on insulin resistance in females with polycystic ovarian syndrome: A randomized controlled trial

Sex-specific increases in myostatin and SMAD3 contribute to obesity-related insulin resistance in human skeletal muscle and primary human myotubes.

The purpose of the present study was to determine the effects of obesity and biological sex on myostatin expression in humans and to examine the direct effects of myostatin, SMAD2, and SMAD3 on insulin signaling in primary human skeletal muscle cells (HSkMCs). For cohort 1, 15 lean [body mass index (BMI): 22.1 ± 0.5 kg/m2; n = 8 males; n = 7 females] and 14 obese (BMI: 40.6 ± 1.4 kg/m2; n = 7 males; n = 7 females) individuals underwent skeletal muscle biopsies and an oral glucose tolerance test. For cohort 2, 14 young lean (BMI: 22.4 ± 1.9 kg/m2; n = 6 males; n = 8 females) and 14 obese (BMI: 39.3 ± 7.9 kg/m2; n = 6 males; n = 8 females) individuals underwent muscle biopsies for primary HSkMC experiments. Plasma mature myostatin (P = 0.041), skeletal muscle precursor myostatin (P = 0.048), and skeletal muscle SMAD3 (P = 0.029) were elevated in obese females compared to lean females, and plasma mature myostatin (r = 0.58, P = 0.029) and skeletal muscle SMAD3 (r = 0.56, P = 0.037) were associated with insulin resistance in females but not males. Twenty-four hours of myostatin treatment impaired insulin signaling in primary HSkMCs derived from females (P < 0.024) but not males. Overexpression of SMAD3, but not SMAD2, impaired insulin-stimulated AS160 phosphorylation in HSkMCs derived from lean females (-27%, P = 0.040), whereas silencing SMAD3 improved insulin-stimulated AS160 phosphorylation and insulin-stimulated glucose uptake (25%, P < 0.014) in HSkMCs derived from obese females. These results suggest for the first time that myostatin-induced impairments in skeletal muscle insulin signaling are sex specific and that increased body fat in females is associated with detrimental elevations in myostatin and SMAD3, which contribute to obesity-related insulin resistance.NEW & NOTEWORTHY Obesity is considered a main risk factor for the development of insulin resistance and type 2 diabetes. The present study utilizes in vivo and in vitro experiments in human skeletal muscle to demonstrate for the first time that females are inherently more susceptible to myostatin-induced insulin resistance, which is further enhanced with obesity due to increased myostatin and SMAD3 expression.

Elderly rats fed with a high-fat high-sucrose diet developed sex-dependent metabolic syndrome regardless of long-term metformin and liraglutide treatment.

The study aimed to determine the effectiveness of early antidiabetic therapy in reversing metabolic changes caused by high-fat and high-sucrose diet (HFHSD) in both sexes. Elderly Sprague-Dawley rats, 45 weeks old, were randomized into four groups: a control group fed on the standard diet (STD), one group fed the HFHSD, and two groups fed the HFHSD along with long-term treatment of either metformin (HFHSD+M) or liraglutide (HFHSD+L). Antidiabetic treatment started 5 weeks after the introduction of the diet and lasted 13 weeks until the animals were 64 weeks old. Unexpectedly, HFHSD-fed animals did not gain weight but underwent significant metabolic changes. Both antidiabetic treatments produced sex-specific effects, but neither prevented the onset of prediabetes nor diabetes. Liraglutide vested benefits to liver and skeletal muscle tissue in males but induced signs of insulin resistance in females.

1176-P: Maternal Hyperglycemia Leads to Distinct Differences in Metabolism and Pancreatic Beta-Cell Function in Male and Female Offspring

Maternal hyperglycemia is a major risk factor for future T2D risk in the offspring. To better understand T2D pathogenesis in this context, we used a mouse model of hyperglycemia induced by high-fat, high-sugar (HFHS) feeding from before mating through to weaning. This resulted in increased adiposity, reduced insulin sensitivity, hyperinsulinemia and impaired glucose tolerance pre-pregnancy. Pregnancy further worsened the metabolic health of dams resulting in reduced insulin levels in addition to glucose intolerance at gestational day 16. By weaning, HFHS-fed dams had fasting hyperglycemia. Maternal hyperglycemia had no impact on offspring body weight and composition at postnatal day 2. However, male offspring of HFHS-fed dams experienced decelerated postnatal growth in the first 2 weeks of life followed by catch-up growth by weaning. Despite comparable body weight, relative fat mass was increased and relative lean mass decreased from 3 to 8 weeks of age in exposed offspring. In males, this was not linked to changes in food intake and metabolic activity measured at 7 weeks. In contrast, daily energy expenditure was increased in female offspring of hyperglycemic dams. At 8 weeks old, despite normal glucose tolerance and insulin sensitivity, male offspring of HFHS-fed dams were hyperinsulinemic during a glucose tolerance test. In contrast, female offspring had reduced insulin sensitivity and higher plasma insulin concentration at baseline and 45 min. Interestingly, insulin secretion was increased only in islets from male offspring characterised by a marked increase in 1st phase and a trend towards higher 2nd phase secretion. Insulin secretion in response to potassium chloride was also increased in these islets. Thus, our data suggest that there are sex-specific mechanisms contributing to future T2D risk in offspring exposed to maternal hyperglycemia with primary hyperinsulinemia being an early feature in males and insulin resistance in females. Disclosure S.E.O'hara: None. K.M.Gembus: None. G.S.Clarke: None. A.J.Page: None. L.M.Nicholas: None. Funding National Health and Medical Research Council of Australia (GNT1092158)

Endothelial MRs mediate Western diet-induced lipid disorders and skeletal muscle insulin resistance in females.

Consumption of a Western diet (WD) consisting of excess fat and carbohydrates activates the renin-angiotensin-aldosterone system, which has emerged as an important risk factor for systemic and tissue insulin resistance. We recently discovered that activated mineralocorticoid receptors (MRs) in diet-induced obesity induces CD36 expression, increases ectopic lipid accumulation, and results in systemic and tissue insulin resistance. Here, we further investigated whether endothelial cell (EC) specific MR (ECMR) activation participates in WD-induced ectopic skeletal muscle lipid accumulation, insulin resistance and dysfunction. Six-week-old female ECMR knockout (ECMR-/-) and wild type (ECMR+/+) mice were fed either a WD or a chow diet for 16 weeks. ECMR-/- mice were found to have decreased WD-induced in vivo glucose intolerance and insulin resistance at 16-weeks. Improved insulin sensitivity was accompanied by increased glucose transporter type 4 (Glut4) expression in conjunction with improved soleus insulin metabolic signaling in phosphoinositide 3-kinases/protein kinase B and endothelial nitric oxide synthase activation. Additionally, ECMR-/- also blunted WD-induced increases in CD36 expression and associated elevations in soleus free fatty acid, total intramyocellular lipid content, oxidative stress, and soleus fibrosis. Moreover, in vitro and in vivo activation of ECMR increased EC derived exosomal CD36 that was further taken up by skeletal muscle cells, leading to increased skeletal muscle CD36 levels. These findings indicate that in the context of an obesogenic WD, enhanced ECMR signaling increases EC derived exosomal CD36 resulting in increased uptake and elevated concentrations of CD36 in skeletal muscle cells, contributing to increased lipid metabolic disorders and soleus insulin resistance.

Review of Novel Potential Insulin Resistance Biomarkers in PCOS Patients-The Debate Is Still Open.

Research on proteins and peptides that play roles in metabolic regulation, which may be considered potential insulin resistance markers in some medical conditions, such as diabetes mellitus, obesity and polycystic ovarian syndrome (PCOS), has recently gained in interest. PCOS is a common endocrine disorder associated with hyperandrogenemia and failure of ovulation, which is often accompanied by metabolic abnormalities, including obesity, dyslipidemia, hyperinsulinemia, and insulin resistance. In this review, we focus on less commonly known peptides/proteins and investigate their role as potential biomarkers for insulin resistance in females affected by PCOS. We summarize studies comparing the serum fasting concentration of particular agents in PCOS individuals and healthy controls. Based on our analysis, we propose that, in the majority of studies, the levels of nesfastin-1, myonectin, omentin, neudesin were decreased in PCOS patients, while the levels of the other considered agents (e.g., preptin, gremlin-1, neuregulin-4, xenopsin-related peptide, xenin-25, and galectin-3) were increased. However, there also exist studies presenting contrary results; in particular, most data existing for lipocalin-2 are inconsistent. Therefore, further research is required to confirm those hypotheses, as well as to elucidate the involvement of these factors in PCOS-related metabolic complications.

Effect of 6 weeks Pilates training along with dill supplementation on serum concentrations of nesfatin-1, lipocalin-2, and insulin resistance in females with overweight and obesity: A randomized controlled trial.

This study aimed to investigate the effect of 6 weeks' pilates training along with dill supplementation on serum concentrations of nesfatin-1, lipocaline-2, and insulin resistance in females with overweight and obesity. In this randomized controlled trial study, 45 overweight and obese females are randomly assigned to four groups: Pilates training + dill group (PDG) (n = 12), pilates training + placebo group (PPG) (n = 11), dill supplementation group (DG) (n = 11), and placebo group (PG) (n = 11). Participants of PDG and PPG performed pilates training for 6 weeks (60 min, 3 sessions per week). PDG and DG received dill tablet (three times a day, 6 weeks). Anthropometric measurements, glycemic markers, and blood samples were assessed before (pretest) and after (posttest) 6 weeks of intervention. Results showed a significant increase in serum concentrations of nesfatin-1 in PDG compared to pretest (P = 0.001). Differences in the serum concentrations of nesfatin-1 in PDG were greater than PPG, DG, and PG (P = 0.01). Furthermore, results found in significant reduction in serum concentrations of lipocalin-2, body mass index (BMI), and waist-hip ratio (WHR) in PDG, PPG, and DG as compared to pretest (P > 0.05). Fasting glucose plasma (FGP) was significantly decreased in all three intervention groups PDG (P < 0.001), PPG (P < 0.001), and DG (P < 0.001) as compared to pretest. Differences in FGP were significantly higher in PDG than PPG, DG, and PG (P = 0.001). A significant reduction was found for insulin only in PDG after 6 weeks of intervention as compared to pretest (P = 0.03). Insulin resistance significantly decreased in PDG (P = 0.03) and PPG (P = 0.04) as compared to pretest. Body fat percent (BFP) was significantly decreased in PDG (P = 0.003), PPG (P = 0.006), and DG (P = 0.01). However, there were no significant inter-group differences in insulin resistance, insulin, serum concentrations of lipocalin-2, BMI, BFP, and WHR after 6 weeks of Pilates training along with dill supplementation (P > 0.05). We concluded that 6 weeks of Pilates training along with dill may be beneficial for improvements in serum concentrations of nesfatin-1 and FGP.

The Relationship between Insulin Resistance and Spatial QRS-T Angle in American Adults.

Insulin resistance can impair the electrical conductivity of the heart. Spatial QRS-T axis reflects ventricular depolarization and repolarization. The relationship between insulin resistance and spatial QRS-T angle has not been examined in the general population. We examined the relationship between insulin resistance and spatial QRS-T angle in an American population-based sample. We used data collected from the National Health and Nutrition Examination Survey III (NHANES III), and a directed acyclic graph to select confounders. We fitted logistic regression models and adjusted for the effect of the confounders. We stratified all analyses by gender. The odds ratios (OR) of the abnormal QRS-T angle and their 95% confidence intervals (CI) for females and males were 1.08 (1.03-1.16) and 1.03 (0.96-1.11), respectively. A 5-unit increase in insulin resistance in females increased the odds of an abnormal QRS-T angle by 47% (OR = 1.47, 95% CI, 1.10-2.10); in males, a 5-unit increase in insulin resistance increased the OR by 17% (OR = 1.17, 95% CI, 0.82-1.70). Spatial QRS-T angle may be associated with insulin resistance, especially in women. The individuals with a higher insulin resistance value had higher odds for major adverse cardiovascular events. Nevertheless, the results of this study should be verified in prospective studies.

The Association of Visceral Adiposity Index with Insulin Resistance in Adults with Prediabetes

Visceral adiposity mediates insulin resistance, but their association among adults with prediabetes is scarce in the literature. This study is aimed to determine the association of visceral adiposity index (VAI) with insulin resistance in adults with prediabetes. This cross-sectional study was done among 117 adults with newly detected prediabetes [m/f; 23/94; mean ± SD: Age 36.30 ± 9.99 years, BMI 28.89 ± 4.35 kg/m2] based on American Diabetes Association 2018 criteria and 141 matched healthy controls [m/f: 28/113; mean ± SD: 35.30 ± 6.88 years, BMI 25.03 ± 4.58]. Waist circumference, body mass index, fasting triglyceride, HDL cholesterol, fasting blood glucose and insulin were measured in each group to calculate VAI and homeostatic model assessment of insulin resistance (HOMA-IR). People with prediabetes had significantly higher median value of VAI {3.08 (2.26) vs. 1.86 (2.31); p 1) (98.3% vs. 85.8%; p < 0.001) than the control population. HOMA-IR level was significantly higher in prediabetes with high VAI (cut-off of 2.64) than control with normal VAI [2.78 (2.22, 4.15) vs. 2.20 (1.53, 3.36); p = 0.002]. VAI was positively correlated with HOMA-IR in females with prediabetes (r = 0.299, p = 0.003). VAI had predictive association with prediabetes [OR (95% CI: 9.504 (2.173, 41.576); p = 0.03] and high insulin resistance (HOMA-IR ≥ 2.6) in females with prediabetes [OR (95% CI) = 3.50 (1.476, 8.297); p = 0.004] only. It could satisfactorily discriminate prediabetes in both sexes (male: AUC = 0.767, p = 0.001; female: AUC = 0.641, p < 0.001) and high insulin resistance in females with prediabetes (AUC = 0.641; p = 0.019) only. So, VAI was associated with prediabetes and insulin resistance only in females with prediabetes.

Elevated serum levels of galectin-3 binding protein are associated with insulin resistance in non-diabetic women after menopause

ObjectiveGalectin-3 binding protein (Gal-3BP) is one of the major fucosylated glycoprotein family members and has recently been implicated in non-alcoholic fatty liver disease, hyperlipaemia and coronary artery disease. Here, we analysed the serum concentrations of Gal-3BP in menopausal women to evaluate the association of circulating Gal-3BP and insulin resistance in females after menopause. Materials and methodsWe evaluated serum levels of Gal-3BP in sixty-two non-diabetic women with menopausal status for at least one year. The clinical features, biochemical profiles and homeostasis model assessment of insulin resistance (HOMA-IR) indices were obtained routinely. ResultsGal-3BP levels increased in women with higher HOMA-IR indices and were positively correlated with HOMA-IR indices. The Gal-3BP level was also an independent risk factor for a high HOMA-IR index and showed the most influence on the HOMA-IR index compared to fasting plasma glucose, triglyceride, age and body mass index. The cut-off value of the serum Gal-3BP level was 2234.32 ng/ml, with areas under the ROC curve (AUCs) of 0.68 (HOMA-IR index 1.5), 0.81 (HOMA-IR index 2.0) and 0.93 (HOMA-IR index 2.5). ConclusionSerum levels of Gal-3BP are associated with impaired insulin sensitivity in non-diabetic menopausal women.

Relationship of obesity to adipose tissue insulin resistance

AimsThis study aimed to examine the association of different anatomical forms of obesity with adipose tissue insulin resistance and to assess the diagnostic value and contribution of obesity to adipose...

Effect of diet in females (F1) from prenatally undernourished mothers on metabolism and liver function in the F2 progeny is sex-specific

Poor maternal nutrition sensitises to the development of metabolic diseases and obesity in adulthood over several generations. The prevalence increases when offspring is fed with a high-fat (HF) diet after weaning. This study aims to determine whether such metabolic profiles can be transmitted to the second generation and even aggravated when the mothers were exposed to overnutrition, with attention to potential sex differences. Pregnant Wistar rats were subjected to ad libitum (control) or 70% food-restricted diet (FR) during gestation (F0). At weaning, F1 females were allocated to three food protocols: (1) standard diet prior to and throughout gestation and lactation, (2) HF diet prior to and standard diet throughout gestation and lactation, and (3) HF diet prior to and throughout gestation and lactation. F2 offspring was studied between 16 and 32 weeks of age. FR-F2 offspring on standard diet showed normal adiposity and had no significant metabolic alterations in adulthood. Maternal HF diet resulted in sex-specific effects with metabolic disturbances more apparent in control offspring exposed to HF diet during gestation and lactation. Control offspring displayed glucose intolerance associated with insulin resistance in females. Female livers overexpressed lipogenesis genes and those of males the genes involved in lipid oxidation. Gene expression was significantly attenuated in the FR livers. Increased physical activity associated with elevated corticosterone levels was observed in FR females on standard diet and in all females from overnourished mothers. Maternal undernutrition during gestation (F0) improves the metabolic health of second-generation offspring with more beneficial effects in females.

Adipocyte ACLY Facilitates Dietary Carbohydrate Handling and Protects Against Insulin Resistance in Females

Sugars and refined carbohydrates are major components of the modern diet. ATP-citrate lyase (ACLY) is upregulated in adipocytes in response to carbohydrate consumption and generates acetyl-CoA for both lipid synthesis and acetylation reactions. Here we investigated the role of ACLY in the metabolic and transcriptional responses to carbohydrates in adipocytes, and unexpectedly uncovered a sexually dimorphic function in maintaining systemic metabolic homeostasis. When fed a high sucrose diet, AclyFAT-/- females exhibit a lipodystrophy-like phenotype, with minimal fat accumulation, insulin resistance, and hepatic lipid accumulation, while AclyFAT-/- males have only mild metabolic phenotypes. We find that ACLY is crucial for nutrientdependent ChREBP activation in adipocytes and plays a key role particularly in females in the storage of newly synthesized fatty acids in adipose tissue. The data indicate that adipocyte ACLY is important in females for the systemic handling of dietary carbohydrates and for the preservation of metabolic homeostasis.

Effects of 17β-Estradiol and Androgen on Glucose Metabolism in Skeletal Muscle.

Diabetes develops predominantly in males in experimental models, and extensive evidence suggests that 17β-estradiol (E2) modulates progression of diabetes in humans. We previously developed a severely diabetic transgenic (Tg) mouse model by β-cell-specific overexpression of inducible cAMP early repressor (ICER) and found that male ICER-Tg mice exhibit sustained severe hyperglycemia, but female ICER-Tg mice gradually became normoglycemic with aging. This implies that differences in circulating androgen and E2 levels might influence skeletal muscle glucose uptake and glycemic status. Here we examined whether a decrease of androgen or E2 excess can improve muscle glucose uptake in hyperglycemic male ICER-Tg mice and, conversely, whether a decrease of E2 or androgen excess can elevate blood glucose levels and impair muscle glucose uptake in normoglycemic female ICER-Tg mice. We treated hyperglycemic male ICER-Tg mice with orchiectomy (ORX) or ORX+E2 pellet implantation and normoglycemic female ICER-Tg mice with ovariectomy (OVX) or OVX+5α-DHT pellet implantation to alter the androgen to E2 ratio. ORX+E2 treatment of male ICER-Tg mice caused a rapid drop in blood glucose via both a dramatic increase of β-cells and significantly improved muscle glucose uptake due to the induction of glucose transporter type 4 (GLUT4) expression and translocation of GLUT4 to the cell membrane. In contrast, OVX+5α-DHT-treated female ICER-Tg mice showed an elevation of blood glucose without any decrease of β-cells; instead, they showed decreased muscle glucose uptake due to decreased activation of serine/threonine-specific protein kinase AKT and GLUT4 expression. These findings suggest that androgen (5α-DHT) promotes insulin resistance in females, whereas E2 improves insulin sensitivity in severely diabetic male mice.

Differential pattern for regulating insulin secretion, insulin resistance, and lipid metabolism by osteocalcin in male and female T2DM patients.

BackgroundOsteocalcin has been reported to be relevant to glucose and lipid metabolism, indicating it may stimulate insulin secretion and improve insulin resistance. Yet the difference between male and female patients is still not clear.We aimed to investigate the difference in serum osteocalcin, and its association with glucose, lipid metabolism, pancreatic function, insulin sensitivity, and resistance in male and female middle-aged and elderly type 2 diabetic (T2DM) patients.Material/Methods739 T2DM patients were included. After measurement of body mass index (BMI), the levels of fasting plasma glucose (FPG), insulin (FINS), C peptide (FC-P), 2-h post-OGTT plasma glucose (2h-PG), HbA1C, and osteocalcin were determined. Homeostasis model assessment of β-cell function (HOMA-%B), homeostasis model assessment of insulin sensitivity (HOMA-%S), and homeostasis model assessment of insulin resistance (HOMA-IR) were calculated.ResultsFemales had higher osteocalcin concentration than males (P<0.05). In males, serum osteocalcin was negatively correlated with HbA1C, FPG, and 2-h PG (P<0.05), but positively with 2-h post-OGTT C peptide (2hC-P), 2-h post-OGTT serum insulin (2h-INS), and HOMA-%B (P<0.05). In females, serum osteocalcin was negatively correlated with HbA1C, FPG, triglyceride (TG), and HOMA-IR (P<0.05), but positively with 2-h C-P, 2-h INS, HOMA-%B, HOMA-%S, and high-density lipoprotein (HDL) (P<0.05). In all subjects, serum osteocalcin was inversely correlated with HbA1C, FPG, and 2-h PG (P<0.05), but positively with 2-h C-P, 2-h INS, HDL, and HOMA-%B (P<0.05).ConclusionsOsteocalcin might improve glucose metabolism through enhancing insulin secretion in males, and through increasing insulin secretion and improving insulin resistance in females with T2DM. Osteocalcin probably also plays an important role in lipid metabolism.

Role of surrogate markers in assessment of insulin resistance in females with thyroid disorders

IntroductionThyroid status is known to affect insulin sensitivity although conflicting data have been reported regarding hypothyroid and hyperthyroid states. Assessment of insulin resistance is difficult, therefore we compared homeostasis model assessment (HOMA), glucose to insulin (G:I) ratio, glucose to C-peptide (G:C) ratio and ferritin of hypothyroid and hyperthyroid subjects with euthyroid, euglycemic subjects. MethodsThe study group comprised of 40 hypothyroid, 25 hyperthyroid female subjects and 40 euthyroid controls. Serum samples of all the patients were assayed for thyroid profile, glucose, Insulin, C-peptide and ferritin. Homeostasis model of assessment (HOMA-IR), (G:I), (G:C) and ferritin were employed as surrogate measures to assess the level of insulin resistance. The area under the curves for the surrogate markers was determined from the receiver operating characteristics (ROC) curves for the hypothyroid and hyperthyroid patients. ResultsPatients with hypothyroidism demonstrated insulin resistance as observed by the higher HOMA-IR and G:I ratio as compared to the controls whereas insulin resistance was not detected in the hyperthyroid patients in our study. ConclusionThyroid dysfunction attributes to deranged glucose metabolism. Assessment of the surrogate markers might prove to be beneficial in detecting insulin resistance at the incipient stages and subsequent management.

Is Plasma Homocysteine Level Associated With Metabolic Syndrome Components in Adolescents?

This study investigated whether serum homocysteine (Hcy) level is associated with metabolic syndrome components, including high waist circumference (WC), hypertriglyceridemia, low high-density lipoprotein-cholesterol (HDL-C), elevated systolic blood pressure (SBP), and insulin resistance (IR) in adolescents living in Central Anatolia, Turkey. The data of The Prevalence of Metabolic Syndrome Among Adolescents Study, a cross-sectional study carried out in two of the central and ten outlying districts of Kayseri was used. Components of metabolic syndrome were modified from the Adult Treatment Panel III (ATP III). A multivariate regression model was developed to examine the relationships between the homocysteine (Hcy) level and metabolic syndrome components. Hyperhomocysteinemia (HH) was defined as level of Hcy > or = 15 micromol/L. Mean plasma Hcy level of adolescents with metabolic syndrome was found to be 11.8 +/- 5.0 micromol/L. Although the Hcy level of females (11.4 +/- 5.5 micromol/L) was lower than that of males (12.0 +/- 4.7 micromol/L), the difference was not statistically significant (P > 0.05). In all, 40.5% of adolescents had Hcy levels between 10 and 15 micromol/L (mild HH) and 17.7% of adolescents had Hcy levels of > or = 15 micromol/L. The Hcy level was negative and weakly correlated with insulin resistance in females (r = -0.319, P = 0.058) and negative strongly correlated with SBP in males (r = - 0.385, P = 0.011). There were no associations between Hcy level and other components of metabolic syndrome. An elevated plasma Hcy level is not considered to be related to components of metabolic syndrome. But HH may be an independent risk factor, especially for diabetic adolescents or those who have cardiovascular events as in adults.

Association Between the Number of Cardiovascular Risk Factors and Each Risk Factor Level in Elementary School Children

Little is known regarding the association between numbers of cardiovascular (CV) risk factors and the level of each risk factor in elementary school children based on a longitudinal study. A descriptive study of 319 obese children aged 6-11 years who participated in a screening program for comorbidity of obesity between 2003 and 2005, and who participated in consecutive years thereafter, was performed. Abdominal obesity, hypertension, dyslipidemia (low high-density lipoprotein-cholesterol levels and/or high triglyceride levels), and raised fasting glucose levels were used as the CV risk factors. Metabolic syndrome and each CV risk factor were defined using the criteria newly established by a Task Force financed by the Health and Labour Science Research in Japan. An increase in the total number of CV risk factors implied a worsening of each CV risk factor level over a 1-year interval, and vice versa. Abdominal obesity in males and insulin resistance in females were prevalent in children who were at elementary school level. We should assess not only obesity but all CV risk factor levels, because a cluster of risk factors implies a worsening of the individual risk factor levels in children as young as those in elementary school.

Uric acid: A surrogate of insulin resistance in older women

Objectives The relationship between serum uric acid (UA) and cardiovascular disease has been debated extensively and no conclusion has been reached yet. The main purpose of this study was to explore the sex-different relationship among insulin resistance, metabolic syndrome (MS) and hyperuricemia. Methods A community-based prospective study was conducted among people aged over 40 years in I-Lan County, Taiwan. A complete history taking, physical examination and laboratory tests were performed for each subject by the well-trained research staff. Insulin resistance was determined by the homeostasis model assessment (HOMA-IR). Serial comparisons were performed to evaluate the associations between MS, insulin resistance and hyperuricemia in both sexes. Results A total of 852 subjects (mean age = 64.6 ± 11.3 years, 56.7% female) were enrolled. The prevalence of obesity, hyperuricemia, chronic kidney disease (CKD), insulin resistance and MS was 42.2, 31.2, 30.9, 36.0 and 47.5%, respectively. Subjects with MS were significantly older (63.4 ± 10.0 years versus 60.4 ± 12.4 years, P = 0.019), higher in body mass index (BMI) (26.3 ± 3.5 kg/m 2 versus 23.6 ± 3.0 kg/m 2, P < 0.001), serum UA (6.1 ± 2.1 mg/dl versus 5.5 ± 1.7 mg/dl, P = 0.003), HOMA-IR (2.7 ± 3.4 versus 1.0 ± 0.8, P < 0.001) and lower in glomerular filtration rate (GFR) (66.3 ± 17.7 ml/min/1.73 m 2 versus 72.0 ± 15.2 ml/min/1.73 m 2, P = 0.001). Male gender, CKD, BMI > 23 kg/m 2 and insulin resistance were all independent risk factor for hyperuricemia with the covariate of age. When age and BMI were controlled, females had significantly higher prevalence of CKD and insulin resistance, but less hyperuricemia than males ( P all < 0.05). Adjusted for age, BMI and GFR, hyperuricemia and MS were both independent risk factors for insulin resistance in females ( P = 0.006, <0.001, respectively). In males, MS remained significantly associated with insulin resistance ( P = 0.002) but not hyperuricemia ( P = 0.813). When age, BMI and GFR were controlled, serum UA was positively related to HOMA-IR in females ( γ = 0.117, P = 0.012), but not in males ( P = 0.93). Conclusion A positive association was identified between serum UA and insulin resistance in older women but not in men. Studies related to insulin resistance may be needed when hyperuricemia was identified in older women.