Adherence to a low‐fat vs. low‐carbohydrate diet differs by insulin resistance status

Previous research shows diminished weight loss success in insulin‐resistant (IR) women assigned to a low‐fat (LF) diet compared to those assigned to a low‐carbohydrate (LC) diet. These secondary analyses examined the relationship between insulin‐resistance status and dietary adherence to either a LF‐diet or LC‐diet among 81 free‐living, overweight/obese women [age = 41.9 ± 5.7 years; body mass index (BMI) = 32.6 ± 3.6 kg/m²]. This study found differential adherence by insulin‐resistance status only to a LF‐diet, not a LC‐diet. IR participants were less likely to adhere and lose weight on a LF‐diet compared to insulin‐sensitive (IS) participants assigned to the same diet. There were no significant differences between IR and IS participants assigned to LC‐diet in relative adherence or weight loss. These results suggest that insulin resistance status may affect dietary adherence to weight loss diets, resulting in higher recidivism and diminished weight loss success of IR participants advised to follow LF‐diets for weight loss.     

Genetic determination of adiponectin and its relationship with body fat topography in multigenerational families of African heritage

Adiponectin, an adipose-specific protein, is negatively associated with adiposity, insulin sensitivity, and diabetes. Very few studies have examined the role of heredity in the regulation of adiponectin and its association with body fat among individuals of African heritage. Thus, we measured fasting serum adiponectin levels by radioimmunoassay and body composition by dual-energy x-ray absorptiometry (DEXA) in 402 individuals aged 18 to 103 years belonging to 7 multigenerational families of African heritage in the relatively homogeneous island population of Tobago. Heritability of adiponectin was 33.2% (P < .01), and age, sex, and body mass index explained 23.4% of the variance in adiponectin. Sex-specific heritability was significant in men (heritability, 34%; P < .05), but not in women. The inverse associations between body mass index and percentage of body fat and adiponectin, independent of age and height, were much stronger in women (all P values <.001) than in men. However, percentage of trunk fat was consistently strongly associated with adiponectin in both men (r = -0.40, P < .001) and women (r = -0.44, P < .001), independent of age and height. This study suggests that genetic factors are a significant source of interindividual differences in circulating adiponectin among Afro-Caribbeans. Adiponectin may serve as a promising quantitative intermediate trait in studies designed to map the genes underlying diabetes and obesity in this population.     

Intra-abdominal fat is associated with decreased insulin sensitivity in healthy young men

To distinguish the relative role of intra-abdominal and subcutaneous abdominal fat in metabolic aberrations in upper body fat localization, we measured the relationship between regional fat distribution and insulin sensitivity in nine young men (28.6 +/- 0.7 years; body mass index [BMI], 24.7 +/- 1.3 kg/m2). Regional fat distribution was measured by anthropometric measurement and computed tomography (CT). Insulin sensitivity was measured by euglycemic hyperinsulinemic glucose clamp. Insulin sensitivity, expressed as the ratio of rate of glucose utilization to the mean plasma insulin concentration during the second hour of glucose clamp (M/I) was negatively correlated with BMI (r = -.91, P less than .001), waist to hip girth ratio (WHR) (r = -.80, P less than .01), subcutaneous abdominal fat area (r = -.90, P less than .001), and intra-abdominal fat area (r = -.88, P less than .01). Stepwise forward regression analysis showed that in addition to BMI, intra-abdominal fat area was a significant correlate of decrease in insulin sensitivity. These findings suggest that intra-abdominal fat play an important role in decreasing insulin sensitivity, even in healthy young men.     

Plasma adiponectin and insulin sensitivity in overweight and normal-weight middle-aged premenopausal women

Adiponectin has been reported to regulate systemic insulin sensitivity as a part of a broader control mechanism in energy balance. However, it is not clear whether adiponectin exerts its positive effects on insulin sensitivity equally in a wide range of obesity. We investigated the association of plasma adiponectin concentration with insulin resistance (IR) in a cross-sectional sample of 98 middle-aged premenopausal women with a wide range of obesity. In addition, we studied the relationship between adiponectin, body composition, and blood biochemical and cardiorespiratory fitness variables. Body composition and fat distribution were measured via dual-energy x-ray absorptiometry in normal-weight (NW) (n = 41, body mass index [BMI] <25 kg/m²) and overweight (OW) (n = 57, BMI ≥25 kg/m²) women. Fasting blood samples were obtained; adiponectin, leptin, insulin, glucose, and insulin-like growth factor-I were measured; and IR index was calculated. The IR index from fasting plasma insulin and plasma glucose levels was estimated using the homeostasis model assessment (HOMA), as follows: fasting plasma insulin (in microliter units per milliliter) × fasting plasma glucose (in millimoles per liter)/22.5. Adiponectin was significantly higher (P = .0001) in NW (14.7 ± 4.7 μg/mL) compared with OW (9.9 ± 3.1 μg/mL) women. Significant differences (P < .003) in body mass, BMI, percentage of fat mass, fat mass, trunk fat, trunk fat-leg fat ratio, leptin, insulin, and HOMA were also observed between NW and OW groups. Leptin was independently related to plasma adiponectin (β = −.259, P = .001) in the overall study group. Plasma adiponectin was only related to trunk fat-leg fat ratio (β = −.242, P = .002) among NW subjects, whereas plasma adiponectin was related to fat-free mass (β = .182, P = .0001) and HOMA (β = −.576, P = .002) among OW women. The inverse relationship between adiponectin and leptin concentrations suggests that leptin may be involved in the regulation of adiponectin in middle-aged premenopausal women. Our data also demonstrate that adiponectin may play an important role in sustaining insulin sensitivity only in OW middle-aged premenopausal women.     

Sibutramine improves fat distribution and insulin resistance, and increases serum adiponectin levels in Korean obese nondiabetic premenopausal women

The aim of this study was to evaluate the effects of sibutramine on body composition and fat distribution, insulin resistance, and serum adiponectin levels in obese women. A total of 28 obese, premenopausal women (mean age, 34.5 +/- 13.7 years; BMI, 31.00 +/- 4.10 kg/m2) was studied before and after 12-week-course of sibutramine (10mg/day). Sibutramine treatment reduced body mass index (P < 0.05) and total body fat (P < 0.05). Abdominal subcutaneous and visceral fat areas (ASFA and AVFA) and mid-thigh low density muscle areas (LDMA) measured by computed-tomography decreased significantly (all, P < 0.05). Insulin resistance (IR) calculated from the homeostasis model assessment (HOMA) method decreased (P < 0.05) and serum adiponectin levels increased significantly (P < 0.05). In our sequential data, the changes of fasting serum insulin levels and the HOMA-IR scores, serum free fatty acids and triglyceride levels, serum adiponectin levels and the mid-thigh LDMA preceded significant changes of body weight, total body fat, and abdominal fat distribution, suggesting sibutramine might improve insulin sensitivity directly by alterations of fatty acid metabolism or secondarily by increasing serum adiponectin levels. Conclusively, sibutramine improved fat distribution and insulin resistance, and increased serum adiponectin levels in Korean obese nondiabetic premenopausal women.     

Thyroid function tests in obese prepubertal children: correlations with insulin sensitivity and body fat distribution

Background/Aims: Elevated thyroid-stimulating hormone (TSH) concentrations in association with normal/slightly elevated free triiodothyronine (fT(3)) and/or free thyroxine (fT(4)) have been consistently found in obese children. To examine relationships between adiposity, insulin sensitivity, and TSH, fT(3) and fT(4). Methods: 240 overweight/obese prepubertal children were studied. Fasting TSH, fT(3), fT(4), glucose, insulin, C-peptide, lipids, leptin and adiponectin were evaluated. Insulin sensitivity and resistance were estimated [quantitative insulin check index (QUICKI), insulin sensitivity index (ISI), and hepatic insulin resistance index]. Body fat was measured by dual-energy X-ray absorptiometry. The central obesity index was calculated as the ratio of fat tissue in the trunk region to fat tissue in the leg region. Results: The multiple regression analysis with age, gender and measures of fatness as covariates showed that QUICKI was the only significant negative predictor of TSH and central obesity index the strongest positive predictor of fT(3), in association with either age or hepatic insulin resistance index, and that the only positive determinant of fT(4) was hepatic insulin resistance index. Conclusions: Reduced insulin sensitivity is associated with augmented TSH and fT(4), while progressive central fat accumulation is strictly related to a parallel increase in fT(3) levels, independently from total body fat. Further studies are needed to understand mechanisms linking thyroid function to insulin sensitivity and body composition in obese children.     

Association of adiponectin and resistin with adipose tissue compartments, insulin resistance and dyslipidaemia

AIM: In this study, we investigated the association of plasma adiponectin and resistin concentrations with adipose tissue compartments in 41 free-living men with a wide range of body mass index (22-35 kg/m(2)). METHODS: Using enzyme immunoassays, plasma adiponectin and resistin were measured. Intraperitoneal, retroperitoneal, subcutaneous abdominal and posterior subcutaneous abdominal adipose tissue masses (IPATM, RPATM, SAATM and PSAATM, respectively) were determined using magnetic resonance imaging. Total adipose tissue mass (TATM) was measured using bioelectrical impedance. Insulin resistance was estimated with the help of homeostasis model assessment (HOMA) score. RESULTS: In univariate regression, plasma adiponectin levels were inversely related to IPATM (r = -0.389, p < 0.05), SAATM (r = -0.500, p < 0.001), PSAATM (r = -0.502, p < 0.001), anterior SAATM (r = -0.422, p < 0.01) and TATM (r = -0.421, p < 0.01). In multiple regression models, adiponectin was chiefly correlated with PSAATM. Plasma adiponectin concentrations were also inversely correlated with HOMA score (r = -0.540, p < 0.001) and triglyceride (r = -0.632, p < 0.001), and positively correlated with high-density lipoprotein cholesterol (r = 0.508, p < 0.001). There were no significant correlations between resistin levels and adipose tissue masses, insulin resistance or dyslipidaemia. CONCLUSIONS: In men, total body fat is significantly correlated with plasma adiponectin, but not with plasma resistin levels. Low plasma adiponectin levels appear to be chiefly determined by the accumulation of posterior subcutaneous abdominal fat mass, as opposed to intra-abdominal fat, and are strongly predictive of insulin resistance and dyslipidaemia.     

Aerobic exercise improves insulin resistance and decreases body fat and serum levels of leptin in patients with hepatitis C virus

Aim: Hepatitis C virus infection often complicates glucose intolerance, which can be caused by insulin resistance. Aerobic exercise can improve insulin resistance and decrease body fat in patients with diabetes. The aim of the present study is to clarify whether aerobic exercise improves insulin resistance and decreases body fat in patients with chronic hepatitis C (CH‐C). Methods: Seventeen patients with CH‐C received nutrition education at entry and every two months thereafter. The following were evaluated before and after 6 months of walking at least 8000 steps/day monitored using a pedometer that started 2 months after entry: body composition, fat and muscle weight, visceral and subcutaneous fat areas (VFA and SFA, respectively), liver function tests, the Homeostatic Model of Assessment of Insulin Resistance (HOMA‐IR), serum tumor necrosis factor‐alpha (TNF‐α), interleukin (IL)‐6, adiponectin, leptin and the Short Form‐36. Results: Fifteen of the 17 patients completed the study protocol. Bodyweight, body mass index, fat weight, VFA, SFA, alanine aminotransferase level and HOMA‐IR were significantly decreased at the end of the study (P = 0.004, =0.004, =0.008, =0.041, =0.001, =0.023 and =0.002, respectively). Serum levels of TNF‐α, IL‐6 and adiponectin did not change, whereas those of leptin significantly decreased (P = 0.002). Conclusion: Patients with CH‐C could safely walk as aerobic exercise. Furthermore, walking improved insulin resistance and decreased body fat while lowering serum levels of leptin.     

Measurement of liver fat by magnetic resonance imaging: Relationships with body fat distribution, insulin sensitivity and plasma lipids in healthy men

AIM: We compared the use of magnetic resonance imaging (MRI) as a test for liver fat content (LFAT) with proton magnetic resonance spectroscopy (MRS) and investigated its relationship with body fat distribution, insulin sensitivity, plasma lipids and lipoproteins. METHODS: LFAT was quantified by MRI and MRS in 17 free-living, healthy men with a wide range of body mass indexes. Fasting adiponectin was measured by immunoassay and insulin resistance by homeostasis assessment (HOMA) score. Intraperitoneal, retroperitoneal, anterior subcutaneous and posterior subcutaneous abdominal adipose tissue masses (ATMs) were determined by MRI. RESULTS: Measurements of LFAT by MRI and MRS were highly correlated (r = 0.851, p < 0.001). In univariate regression analysis, LFAT by MRI was also significantly correlated with plasma triglycerides (TGs), insulin, HOMA score, carbohydrate intake and the masses of all abdominal adipose tissue compartments (p < 0.05). LFAT was inversely correlated with plasma adiponectin (r = -0.505, p < 0.05). In multivariate linear regression analysis including plasma adiponectin and age, intraperitoneal ATM was an independent predictor of LFAT (beta-coefficient = 0.587, p = 0.024). Moreover, intraperitoneal ATM was also an independent predictor of HOMA score after adjusting for LFAT, plasma adiponectin and age (beta-coefficient = 0.810, p = 0.010). Conversely, LFAT was a significant predictor of plasma TG concentration after adjusting for adiponectin, intraperitoneal ATM, HOMA and age (beta-coefficient = 0.751, p = 0.007). Similar findings applied with LFAT measured by MRS. CONCLUSIONS: These data suggest that MRI is as good as MRS to quantify liver fat content. Our data also suggest that liver fat content could link intraabdominal fat with insulin resistance and dyslipidaemia.     

The reciprocal association of adipocytokines with insulin resistance and C-reactive protein in clinically healthy men

In experimental models, adiponectin improves and tumor necrosis factor alpha (TNF- alpha ) impairs insulin action, and the expression of these adipocytokines seems to have a reciprocal regulation. The aim was to examine whether in a cross-sectional study, associations supporting this concept may be found in 58-year-old clinically healthy men, and also the relation to C-reactive protein (CRP). In 102 men, euglycemic hyperinsulinemic clamp was used to assess glucose infusion rate (GIR). Total body fat (dual-energy x-ray absorptiometry), plasma adiponectin (radioimmunoassay), TNF-alpha , and CRP (enzyme-linked immunosorbent assay) were measured. Adiponectin correlated positively to GIR (r=0.33, P<.001) and negatively to total fat mass (r=-0.29, P=.004), whereas TNF- alpha showed reverse associations (r=-0.31, P<.01, and r=0.31, P<.01). Adiponectin and TNF- alpha were negatively correlated (-0.28, P=.006). An interaction term (TNF- alpha /adiponectin ratio) and body fat together explained 31.3% (P<.001) in GIR variability. The odds ratio for having insulin resistance was 9.3 (95% CI, 2.2-38.9) in subjects with TNF-alpha values above and adiponectin levels below the median, as compared to subjects with TNF- alpha values below and adiponectin levels above the median. Total fat and TNF-alpha , but not adiponectin, were significantly associated with log CRP (R2=20%, P<.001). In conclusion, this study in man showed that plasma adiponectin and TNF-alpha were independently and reversely associated with insulin resistance. C-reactive protein levels were related to TNF-alpha and obesity.     

Retinol-binding protein 4 is associated with insulin resistance and body fat distribution in nonobese subjects without type 2 diabetes

BACKGROUND: Adipose tissue is responsible for releasing various adipokines that have been related to insulin resistance. Understanding the relationship of these adipokines to insulin resistance may foster the development of new treatments for diabetes. OBJECTIVES: The primary objective of this study was to determine whether an association between retinol-binding protein 4 (RBP4) and insulin resistance exists in nonobese individuals without a family history or diagnosis of diabetes. The secondary objective was to determine by a dual energy x-ray absorptiometry scan which adipose tissue depot most closely relates to RBP4 levels. DESIGN: Cross-sectional analysis of 92 study participants ranging in age from 20 to 83 yr was performed. The range of body mass index (BMI) was from 18 to 30 kg/m(2). Exclusion criteria were a BMI greater than 30 kg/m(2), family history of diabetes, or a diagnosis of diabetes. Insulin sensitivity was determined by a hyperinsulinemic euglycemic clamp. Body fat was measured by dual energy x-ray absorptiometry scan. RESULTS: RBP4 values were lower in females (35.8 +/- 1.7 microg/ml) compared with males (39.9 +/- 1.4 microg/ml; P = 0.06). RBP4 levels were found to correlate negatively with insulin sensitivity (r = -0.32; P = 0.002) and positively with age (r = 0.38; P < 0.001). RBP4 levels did not correlate with BMI (r = -0.13; P = 0.22), trunk fat (r = 0.16; P = 0.22), or percent body fat (r = 0.07; P = 0.65). However, RBP4 levels did correlate with percent trunk fat (r = 0.36; P = 0.001). CONCLUSION: These findings indicate a relationship between RBP4, insulin sensitivity, and percent trunk fat in individuals who may not have features of insulin resistance.     

The relationship between plasma adiponectin concentration and insulin resistance is altered in smokers

CONTEXT: Low plasma adiponectin concentrations in smokers may contribute to the adverse consequences that occur in these individuals. OBJECTIVE: The objective of the study was to define the relationship among smoking, plasma adiponectin concentrations, insulin resistance, and inflammation. DESIGN: This was a cross-sectional, observational study with a 2 x 2 factorial design and a prospective longitudinal arm. SETTING: The study was conducted at a general clinical research center. PARTICIPANTS: Apparently healthy smokers (n = 30) and nonsmokers (n = 30), subdivided into insulin resistant (IR) (n = 15) and insulin sensitive (IS) (n = 15) subgroups participated in the study. INTERVENTION: Intervention included pioglitazone administration for 3 months to 12 IR smokers and eight IS smokers. MAIN OUTCOME MEASUres: Measures included fasting plasma adiponectin and C-reactive protein (CRP) concentrations and changes in adiponectin after pioglitazone treatment in IR and IS smokers. RESULTS: Being either a smoker or having insulin resistance was independently associated with lower adiponectin concentrations (P = 0.046 and 0.001, respectively). The difference in mean adiponectin concentration between smokers and nonsmokers did not depend on the insulin resistance status of the subjects. No difference was detected in average CRP concentrations between smokers and nonsmokers (P = 0.18) and between IR and IS subjects (P = 0.13). CRP concentrations were unrelated to adiponectin in smokers (r = -0.05, P = 0.78) and nonsmokers (r = 0.03, P = 0.86). Finally, pioglitazone treatment increased adiponectin concentrations in both IR (P < 0.001) and IS smokers (P = 0.001). CONCLUSIONS: Plasma adiponectin concentrations are lower in smokers and IR subjects and are unrelated to CRP concentrations. These findings suggest that low levels of adiponectin in smokers may be independent of both insulin resistance and a generalized inflammatory response.     

Insulin sensitivity is correlated with subcutaneous but not visceral body fat in overweight and obese prepubertal children

AIM: Our aim was to explore the relationship between insulin sensitivity, body fat distribution, ectopic (liver and skeletal muscle) fat deposition, adipokines (leptin and adiponectin), and inflammation markers (highly sensitive C-reactive protein, IL-6, IL-10, and TNF-alpha) in prepubertal children. SUBJECTS AND METHODS: Thirty overweight and obese children (16 males and 14 females with body mass index z-score range of 1.1-3.2) were recruited. Body fat distribution and fat accumulation in liver and skeletal muscle were measured using magnetic resonance imaging. Insulin sensitivity was assessed by iv glucose tolerance test. RESULTS: Insulin sensitivity was associated with sc abdominal adipose tissue (SAT) (r = -0.52; P < 0.01) and liver fat content (r = -0.44; P < 0.02) but not with visceral abdominal adipose tissue (VAT) (r = -0.193; P value not significant) and fat accumulation in skeletal muscle (r = -0.210; P value not significant). Adipokines, but not inflammation markers, were significantly correlated to insulin sensitivity. VAT correlated with C-reactive protein (r = 0.55; P < 0.01) as well as adiponectin (r = -0.53; P <0.01). Multiple regression analysis showed that only SAT and liver fat content were independently correlated to insulin sensitivity (P < 0.01; 20 and 16% of explained variance, respectively). CONCLUSIONS: In overweight and moderately obese prepubertal children, insulin sensitivity was negatively correlated with SAT and liver fat content. Furthermore, contrary to adults, VAT and inflammation markers were not correlated with insulin sensitivity in children.     

Adiponectin is independently associated with insulin sensitivity in women with polycystic ovary syndrome

OBJECTIVE: The polycystic ovary syndrome (PCOS) is associated with obesity and insulin resistance predisposing to diabetes mellitus type 2 and atherosclerosis. Adiponectin is a recently discovered adipocytokine with insulin-sensitizing and putative antiatherosclerotic properties. The aim of the study was to elucidate determinants of circulating adiponectin levels and to investigate the potential role of adiponectin in insulin resistance in PCOS women. PATIENTS AND MEASUREMENTS: Plasma adiponectin and parameters of obesity, insulin resistance and hyperandrogenism were measured In 62 women with PCOS and in 35 healthy female controls. RESULTS: Both in PCOS and controls, adiponectin levels were lower in overweight or obese women than in normal-weight women, without any difference between PCOS and controls after adjustment for body mass index (BMI). In PCOS and in controls there was a significant correlation of adiponectin with BMI (r = -0.516, P < 0.001), fasting insulin (r = -0.404, P < 0.001), homeostasis model sensitivity (HOMA %S) (r = -0.424, P < 0.001) and testosterone (r = -0.279, P < 0.01), but no correlation with androstenedione (r = -0.112, P = 0.325), 17-OH-progesterone (r =-0.031, P = 0.784) or the LH/FSH ratio (r =-0.033, P = 0.753). Multiple linear regression analysis revealed that BMI and HOMA %S but not testosterone were independently associated with adiponectin plasma levels, explaining 16% (BMI) and 13% (HOMA %S) of the variability of adiponectin, respectively. In PCOS patients insulin sensitivity, as indicated by continuous infusion of glucose with model assessment (CIGMA %S) was significantly correlated with adiponectin (r = 0.55; P < 0.001), BMI (r =-0.575; P < 0.001), waist-to-hip ratio (WHR) (r =-0.48; P = 0.001), body fat mass assessed by dual-energy X-ray-absorptiometry (DEXA) [Dexa-fat (total) (r = -0.61; P < 0.001) and Dexa-fat (trunk) (r = -0.59; P < 0.001)] and with testosterone (r = -0.42; P = 0.001). Multiple linear regression analysis demonstrated that markers of obesity such as BMI, total or truncal fat mass, age and adiponectin were independently associated with CIGMA %S, and that circulating adiponectin accounted for about 18% of the degree of insulin resistance in PCOS. By contrast, testosterone was not a significant factor, suggesting that PCOS per se did not affect insulin sensitivity independent from obesity, age and adiponectin. Metformin treatment for 6 months in insulin-resistant PCOS women (n = 9) had no effect on plasma adiponectin (P = 0.59) despite significant loss of weight and fat mass and improvement in hyperandrogenaemia. CONCLUSIONS: PCOS per se is not associated with decreased levels of plasma adiponectin. However, circulating adiponectin is independently associated with the degree of insulin resistance in PCOS women and may contribute to the development and/or maintenance of insulin resistance independent from adiposity.     

DPP4 activity is related to body weight and central fat in postmenopausal women

AimsDipeptidyl peptidase-4 (DPP4) is a new adipokine increased in central obesity and related to insulin resistance (IR). Postmenopausal (PM) state may be associated with increase in body weight and central fat distribution. We hypothesize that DPP4 is increased in PM women.Materials and methodsTwenty-two non-obese PM and 22 non-obese premenopausal women (PreM), were evaluated. DPP4 activity, lipid profile, HbA1c, FSH, estradiol and sex hormone-binding globulin (SHBG) were measured; an oral glucose tolerance test (OGTT) was performed and IR calculated. Body composition was assessed by dual X-ray absorptiometry (DXA). Correlations between DPP4 and the anthropometric and metabolic variables and body fat distribution were studied.ResultsDPP4 activity was not different between the two groups (PM 5309 ± 650 vs PreM 5387 ± 704 RLU; p = 0,70). In the PM group there was a significant correlation between DPP4 and body weight (r = 0,498; p = 0,03; n = 22) and trunk fat (r = 0,477; p = 0,03; n = 21). There was also a trend for correlation with android (r = 0,418; p = 0,06; n = 21) and total fat (r = 0,409; p = 0,06; n = 21). When stratified by BMI, DPP4 was significantly higher in PM women with BMI ≥25 kg/m² (p = 0,02).ConclusionDPP4 was not increased in PM but is associated with body weight and body fat centralization.     

GnRH脉冲治疗对男性HH患者体脂分布和胰岛素抵抗的影响

目的 研究促性腺激素释放激素(GnRH)脉冲治疗对男性低促性腺激素性性腺功能减退症(HH)患者体脂分布和胰岛素抵抗的影响.方法 选取2013年2月至2015年1月在安徽医科大学第一附属医院就诊的20例男性HH患者为研究对象,测定GnRH脉冲治疗前、后患者性激素、血脂、空腹血糖、空腹胰岛素(FINS)、性激素结合球蛋白(SHBG)等生化指标,计算稳态模型评估-胰岛素抵抗指数(HOMA-IR),并运用双能X线骨密度仪检测全身、躯干及大腿脂肪量和瘦体重,计算所占各自总质量的百分比.结果 经GnRH脉冲治疗6个月后,男性HH患者骨骺闭合人数、卵泡刺激素、黄体生成素、总睾酮、游离睾酮、总瘦体重百分比和躯干瘦体重百分比水平较治疗前增加,FINS、HOMA-IR、总脂肪量百分比和躯干脂肪量百分比水平较治疗前降低(t=-4.169～3.630,P均＜0.05).Pearson相关性分析提示,HOMA-IR与总睾酮(r=-0.676,P=0.032)、游离睾酮(r=-0.731,P=0.016)、躯干瘦体重百分比(r=-0.750,P=0.012)呈负相关,与FINS(r =0.937,P=0.000)、躯干脂肪量百分比(r =0.750,P=0.012)呈正相关.结论 GnRH脉冲治疗可减轻男性HH患者的胰岛素抵抗,改变其体脂分布;睾酮水平和躯干瘦体重百分比的升高、FINS水平和躯干脂肪量百分比的降低可能与胰岛素抵抗的改善有关.     

Adipocytokines, fat distribution, and insulin resistance in elderly men and women

BACKGROUND: The aim of this study was to evaluate the relation between adiponectin and leptin, fat distribution, and insulin resistance in elderly men and women. METHODS: 68 elderly participants (28 men and 40 women) aged 66-77 years, with body mass index (BMI) ranging from 19.83 to 37.18 kg/m2, participated in the study. In all participants, we evaluated BMI, waist and hip circumferences, sagittal abdominal diameter (SAD), fat mass (FM) by dual energy X-ray absorptiometry, fasting and 2-hour glucose, insulin, homeostasis model assessment of insulin resistance (HOMA), leptin, and adiponectin. RESULTS: Elderly women had significantly higher circulating levels of adiponectin and leptin compared to men even after adjusting for age, FM, or waist circumference. In men and women, leptin was positively associated, whereas adiponectin was negatively associated, with BMI, indices of body fat distribution, as well as FM and FM%. Both fasting insulin and HOMA showed significant positive correlation with leptin and negative correlation with adiponectin in both sexes. In a step-wise multiple regression model with HOMA as the dependent variable and age, gender, waist circumference, FM, leptin, and adiponectin as independent variables, waist entered the regression first, explaining 19.7% of HOMA variance, leptin was second, and adiponectin was third, explaining each one an additional 10% of variance. In a multiple linear regression analysis, leptin and adiponectin alone explained up to 38% of HOMA variance. CONCLUSION: Leptin and adiponectin together seem to be strictly related to insulin resistance in elderly people, independently of body fat and body fat distribution.     

High-dose statin therapy does not induce insulin resistance in patients with familial hypercholesterolemia

Abstract Background: Insulin resistance is thought to play a pathophysiological role in the development of atherosclerosis. Decreased adiponectin levels are associated with hyperinsulinemia, insulin resistance, and coronary artery disease. Patients with familial hypercholesterolemia (FH) develop premature atherosclerosis and should be insulin resistant and have low adiponectin levels. Methods: A total of 51 homozygous FH (HoFH) and 20 heterozygous FH (HeFH) patients were studied before and after statin therapy. Twenty normocholesterolemic subjects were controls. Fasting lipograms, glucose, insulin, proinsulin, adiponectin, and high-sensitivity C-reactive protein (hsCRP) were measured. Insulin resistance was calculated with the homeostasis model assessment (HOMA-IR) formula. Carotid intima media thickness (CIMT) was measured as a subclinical marker of atherosclerosis. Results: On multiple regression analysis, the major determinant of insulin resistance measured by HOMA-IR was body mass index (BMI) (r=0.54; P=0.004). On simple linear regression, the highest correlation was with BMI (r=0.39; P=0.0002). Log hsCRP correlated with BMI (r=0.35; P<0.002) and insulin resistance (r=0.22; P=0.05). Low-density lipoprotein cholesterol (LDL-C) and CIMT did not correlate with insulin resistance. Unexpectedly, adiponectin levels were highest in HoFH patients and correlated with LDL-C (r=0.34; P=0.001). No change in the degree of IR was observed with statin therapy. Conclusions: FH patients are not insulin resistant and do not have low adiponectin levels. There was no significant change in insulin resistance with high-dose statin therapy.     

Association between insulin resistance and lean mass loss and fat mass gain in older men without diabetes mellitus

OBJECTIVES: To examine the associations between insulin resistance and changes in body composition in older men without diabetes mellitus. DESIGN: Longitudinal cohort study of older men participating in the Osteoporotic Fractures in Men (MrOS) study. SETTING: Six U.S. clinical centers. PARTICIPANTS: Three thousand one hundred thirty‐two ambulatory men aged 65 and older at baseline. MEASUREMENTS: Baseline insulin resistance was calculated for men without diabetes mellitus using the homeostasis model assessment of insulin resistance (HOMA‐IR). Total lean, appendicular lean, total fat, and truncal fat mass were measured using dual energy X‐ray absorptiometry scans at baseline and 4.6 ± 0.3 years later in 3,132 men with HOMA‐IR measurements. RESULTS: There was greater loss of weight, total lean mass, and appendicular lean mass and less gain in total fat mass and truncal fat mass with increasing quartiles of HOMA‐IR (P<.001 for trend). Insulin‐resistant men in the highest quartile had higher odds of 5% or more loss of weight (odds ratio (OR)=1.88, 95% confidence interval (CI)=1.46–2.43), total lean mass (OR=2.09, 95% CI=1.60–2.73) and appendicular lean mass (OR=1.57, 95% CI=1.27–1.95) and lower odds of 5% or more gain in total fat mass (OR=0.56, 95% CI=0.45–0.68) and truncal fat mass (OR=0.52, 95% CI=0.42–0.64) than those in the lowest quartile. These findings remained significant after accounting for age, site, baseline weight, physical activity, and change in physical activity. These associations were also independent of other metabolic syndrome features and medications. CONCLUSION: Greater lean mass loss and lower fat mass gain occurred in insulin‐resistant men without diabetes mellitus than in insulin‐sensitive men. Insulin resistance may accelerate age‐related sarcopenia.