Insulin In Obese Women Research Articles

Changes of body composition and circulating neopterin, omentin-1, and chemerin in response to thylakoid-rich spinach extract with a hypocaloric diet in obese women with polycystic ovary syndrome: A randomized controlled trial.

This trial evaluated the effects of thylakoid-rich spinach extract supplementation combined with a hypocaloric diet on body composition and serum levels of neopterin, chemerin, and omentin-1 in obese women with polycystic ovary syndrome (PCOS). In this randomized controlled trial, 48 obese women with PCOS, aged 20-45 years old, were recruited and randomly divided into thylakoid (n= 24) and placebo (n= 24) groups. They received a low-calorie diet with 5g/day thylakoid-rich spinach extract or a low-calorie diet with 5 g/day placebo for 12 weeks. The mean age of the participants of the thylakoid group was 31.86 years, and the placebo group was 32.04 years. Thylakoid-rich spinach extract supplementation with a low-calorie diet increased serum levels of omentin-1 (10.90 vs. 3.87 ng/L; p< .001) and decreased fat mass (-5.19 vs. -1.35 kg; p< .001) and serum levels of neopterin (-0.66 vs. -0.38 nmol/L; p= .003) and chemerin (-41.24 vs. -11.26 ng/L; p< .001) in the thylakoid group compared to the placebo group. A significant improvement in omentin-1, chemerin, and neopterin by thylakoid-rich spinach extract supplementation was under the influence of weight change and insulin resistance status throughout the study. A significant decrease in the other anthropometric indices and insulin resistance was also observed in the thylakoid group, compared to the placebo group (p< .001, for all parameters). Thylakoid-rich spinach extract combined with a low-calorie diet increased circulating omentin-1 and decreased fat mass, abdominal obesity, as well as circulating chemerin, neopterin, and insulin in obese women with PCOS.

Elevated Insulin in Obese Women Relates to Low Endogenous Luteinizing Hormone

INTRODUCTION: Obesity is a state of insulin resistance as it is also a state of relative hypogonadotropic hypogonadism. The physiology behind this is still unclear and may be the result of hypothalamic or pituitary factors or pharmacokinetics of gonadotropins. We sought to investigate if insulin, directly or indirectly, suppresses pituitary luteinizing hormone (LH) secretion. METHODS: A luteal phase frequent blood sampling study was undertaken in regularly menstruating obese (n=10) and normal-weight women (n=10). The study included 12 hours of unstimulated monitoring (to evaluate endogenous hypothalamic–pituitary function) with subsequent administration of intravenous bolus of gonadotropin-releasing hormone (to evaluate pituitary sensitivity). Luteinizing hormone was measured with an immunofluorometric assay. Luteinizing hormone pulsatility was evaluated using an objective, widely accepted method. RESULTS: All women were ovulatory. The obese group was significantly older than the normal weight group (32.5±4.7 compared with 27.3±2.6 years, P=.006). Insulin was significantly higher in the obese group than the normal-weight group (21.5 [14.3–28.7] compared with 11.7 [8.9–14.5] mU/L, P=.01). In the 2-hour postprandial period, there was a rise in insulin that was significantly higher (35.6 [17.1–54.1] compared with 16.5 [8.4–24.7] mU/L, P=.04) and LH that trended lower in the obese women (8.1 [3.5–12.7] compared with 4.2 [2.8–5.6] IU/L) (Figure 1).CONCLUSIONS: Higher insulin in obese women may be associated with lower endogenous LH output. A direct role of insulin in suppressing pituitary LH secretion should be further investigated.

Effect of Aerobic Exercise on Serum Concentration of Apelin, TNFα and Insulin in Obese Women.

Apelin is novel adipokine acting on APJ receptor, regulated by insulin and tumor necrosis factor-alpha (TNF-alpha). Plasma apelin levels are increased in obese subjects. The aim of this study was to investigate whether or not the aerobic exercise modifies the elevated plasma apelin levels in obese women. Twenty obese women (BMI 32.2 ± 6.4 kg/m(2)) were selected by random sampling method among obese women. Twelve healthy women with a BMI of 31.7 ± 0.6 kg/m(2) served as control group. The aerobic exercise was performed during 8 weeks, 3 sessions per week. The intensity of the training program proceeded form 50% to 70% in 8 weeks. Results showed that plasma levels of apelin and TNFα were higher in obese individuals compared with the control group. The exercise resulted in significant decrease (P<0.05) of BMI to 29.8± 6.3 kg/m(2) , plasma insulin (8.16 ± 0.73 to 6.58 ± 0.66 µmol/l), apelin (369 ± 25 pg/ml vs 257 ± 12 pg/ml) and TNFα levels (0.66 ± 0.04 pg/ml vs 0.56 ± 0.04 pg/ml). P< 0.05 was considered statistically significant. Exercise can decrease plasma apelin, insulin and TNFα levels in obese women. Regular physical activity causes a decrease in plasma levels of apelin if body mass index and body fat mass simultaneously decreased.

Whole-body protein anabolic response is resistant to the action of insulin in obese women

Background: Obesity is associated with insulin resistance of glucose and lipid metabolism. Objective: We sought to determine the effects of obesity on the insulin sensitivity of protein metabolism. Design: Whole-body [13C]leucine and [3H]glucose kinetics were measured in 9 lean and 10 obese women in the postabsorptive state and during a hyperinsulinemic, euglycemic, isoaminoacidemic clamp. Results: In the postabsorptive state, the leucine endogenous rate of appearance (catabolism), normalized for fat-free mass, was 11% greater and the nonoxidative rate of disappearance (synthesis) was 8% greater in the obese than in the lean women, but net balance was 29% more negative (P < 0.05). Clamp amino acid and glucose infusion rates were significantly lower in the obese women than in the lean women (0.65 ± 0.02 compared with 0.85 ± 0.04 and 5.7 ± 0.3 compared with 9.1 ± 0.5 mg · kg fat-free mass−1 · min−1, respectively; P < 0.0001 for both), and their rates correlated positively (r = 0.635, P = 0.005). During hyperinsulinemia, synthesis was stimulated less and net leucine balance was much lower in the obese women than in the lean women (−0.08 ± 0.06 and 0.30 ± 0.03 μmol · kg fat-free mass−1 · min−1, respectively; P < 0.0001). The percentage change in net leucine balance correlated negatively with all adiposity indexes. Plasma free fatty acids were less suppressed and the respiratory quotient was lower in the obese women than in the lean women. Conclusion: Obese women show a blunted protein anabolic response to hyperinsulinemia that is consistent with resistance to the action of insulin on protein concurrent with that on glucose and lipid metabolism.

Whole-body protein anabolic response is resistant to the action of insulin in obese women

Obesity is associated with insulin resistance of glucose and lipid metabolism. We sought to determine the effects of obesity on the insulin sensitivity of protein metabolism. Whole-body [(13)C]leucine and [(3)H]glucose kinetics were measured in 9 lean and 10 obese women in the postabsorptive state and during a hyperinsulinemic, euglycemic, isoaminoacidemic clamp. In the postabsorptive state, the leucine endogenous rate of appearance (catabolism), normalized for fat-free mass, was 11% greater and the nonoxidative rate of disappearance (synthesis) was 8% greater in the obese than in the lean women, but net balance was 29% more negative (P < 0.05). Clamp amino acid and glucose infusion rates were significantly lower in the obese women than in the lean women (0.65 +/- 0.02 compared with 0.85 +/- 0.04 and 5.7 +/- 0.3 compared with 9.1 +/- 0.5 mg x kg fat-free mass(-1) x min(-1), respectively; P < 0.0001 for both), and their rates correlated positively (r = 0.635, P = 0.005). During hyperinsulinemia, synthesis was stimulated less and net leucine balance was much lower in the obese women than in the lean women (-0.08 +/- 0.06 and 0.30 +/- 0.03 mumol x kg fat-free mass(-1) x min(-1), respectively; P < 0.0001). The percentage change in net leucine balance correlated negatively with all adiposity indexes. Plasma free fatty acids were less suppressed and the respiratory quotient was lower in the obese women than in the lean women. Obese women show a blunted protein anabolic response to hyperinsulinemia that is consistent with resistance to the action of insulin on protein concurrent with that on glucose and lipid metabolism.

Serum Leptin Level in Hypertensive Middle-Aged Obese Women

The mechanism by which adiposity can raise blood pressure is not fully understood. Leptin has been suggested as a possible cause of the arterial hypertension in obese subjects because leptin induces an increase in sympathetic activity. The aim of the present study is to evaluate serum leptin level, blood pressure, lipid profile, blood glucose, and insulin in obese women. Leptin, total cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides were measured. Serum leptin was markedly higher in hypertensive obese women (92.3 ± 22 ng/mL, n = 7) as compared with normotensive obese women (37.7 ± 11 ng/mL, n = 7). Similarly, total cholesterol and LDL cholesterol were significantly elevated in the hypertensive group. No changes were observed in triglycerides and high-density lipoprotein cholesterol concentration between the 2 groups. There were no significant differences in plasma insulin concentration or blood glucose in both groups. In conclusion, our findings suggest a link among dyslipidemia, leptin level, and hypertension that might be relevant to the development of cardiovascular disease in obese subjects.

Leptin Receptor Gene Polymorphisms Are Associated with Insulin in Obese Women with Impaired Glucose Tolerance1

Leptin receptors are present on beta-cells as well as on muscle and fat cells, thus enabling leptin to modulate both insulin secretion and insulin action. Leptin inhibits especially the glucose-stimulated insulin secretion from pancreatic cells. The leptin receptor (LEPR) gene could thus play a role in the regulation of glucose and insulin after an oral glucose load. Therefore, the relationship between LEPR polymorphisms and glucose and insulin response to an oral glucose tolerance test (OGTT) was investigated. Three LEPR polymorphisms (Lys(109)Arg, Gln(223)Arg, and Lys(656)Asn) were typed on genomic DNA of 358 overweight and obese women, aged 18-60 yr. Based on an OGTT, 269 subjects were defined with normal glucose tolerance, and 89 with impaired glucose tolerance (IGT). Associations between genotypes and glucose metabolism were analyzed with a general linear models procedure in pre- and postmenopausal women separately, after adjusting the data for age and fat mass. In postmenopausal women with IGT (n = 24), associations were found with Lys(109)Arg and Lys(656)Asn for fasting insulin (P = 0.05) and with Lys(109)Arg and Gln(223)Arg for the insulin response to an OGTT (P < 0.02). In the same group, trends were found with Lys(656)Asn for fasting glucose as well as in response to the OGTT. In premenopausal women with IGT (n = 65), associations were found with Lys(109)Arg and Lys(656)Asn for overall glucose response to the glucose load. In contrast, no associations with insulin or glucose were found in women with normal glucose tolerance. In conclusion, these data indicate that LEPR polymorphisms are associated with insulin and glucose metabolism in women with impaired glucose homeostasis.

Leptin Receptor Gene Polymorphisms Are Associated with Insulin in Obese Women with Impaired Glucose Tolerance

Leptin Receptor Gene Polymorphisms Are Associated with Insulin in Obese Women with Impaired Glucose Tolerance

Interrelationships between body weight, body fat distribution and insulin in obese women before and after hypocaloric feeding and weight loss.

The effects were investigated of weight loss on the relationship between hyperinsulinemia, body weight and body fat distribution in two groups of women with central-type obesity (CTO) (waist-to-hip ratio WHR greater than 0.85) or peripheral-type obesity (PTO) (WHR less than 0.85). An oral glucose tolerance test was carried out before and after a hypocaloric nutritional treatment lasting 4 months. Both groups were matched for age, body mass index and amount of body fat. At the basal condition, group CTO had fasting and glucose-stimulated insulin levels significantly higher than group PTO; fasting (but not stimulated) C peptide levels were also higher in CTO compared with PTO. Weight and fat loss were significantly higher in CTO than in PTO women. Moreover, unlike PTO, CTO subjects significantly reduced their WHR values. In both groups weight loss led to a significant drop in fasting and glucose-stimulated insulin and C peptide levels. However, PTO women reduced their C peptide levels significantly less than CTO. In conclusion, weight loss only modified body fat distribution in women with CTO, who appeared to be prone to a greater weight loss than the PTO women. Compared to PTO, CTO women were characterized by higher insulin levels and peripheral insulin resistance, which improved during hypocaloric feeding probably due to the combined effect of weight loss and the change in body fat distribution.