Effects of diet and/or exercise on the adipocytokine and inflammatory cytokine levels of postmenopausal women with type 2 diabetes

This study examined the independent and combined effects of diet and exercise on adipocytokine and inflammatory cytokines in postmenopausal women with type 2 diabetes. Using a randomized, controlled design, 33 women (age, 50-70 years) were assigned to diet alone (D), exercise alone (EX), or diet + exercise (D + E) for 14 weeks. Before and after the interventions, blood samples for adipocytokines and inflammatory markers were drawn, a meal test was performed, and abdominal fat distribution was measured by magnetic resonance imaging (MRI). Body weight decreased approximately 4.5 +/- 0.6 kg ( P < .05) after the D and D + E interventions, whereas only small changes in body weight were found with the exercise-alone intervention. Plasma C-reactive protein levels were decreased by approximately 15% with all 3 interventions, whereas leptin levels were reduced with the D and D + E intervention (D: pre = 48.7 +/- 6.0, post = 38.9 +/- 5.0 ng/mL; D + E: pre = 38.5 +/- 6.0, post = 22.9 +/- 5.0 ng/mL; P < .05) with no differences between groups. There was a trend for leptin levels to decrease in the EX group ( P = .06). Plasma resistin levels were not altered by the 3 interventions from pre- to posttreatment (D: pre = 6.9 +/- 0.6, post = 6.2 +/- 0.4 ng/mL; D + E: pre = 5.6 +/- 0.6, post = 5.7 +/- 0.4 ng/mL; E: pre = 6.2 +/- 0.6, post = 5.9 +/- 0.6 ng/mL, P > .05), and no differences in adiponectin and tumor necrosis factor alpha (TNF- alpha ) levels were found. Visceral adipose tissue and tumor necrosis factor alpha were the only predictors of calculated insulin resistance ( P < .05), explaining 43% of the variability. A typically prescribed weight loss program with lifestyle changes resulted in few changes in adipocytokines and inflammatory cytokines in older women with type 2 diabetes, suggesting that dramatic weight loss or clinical interventions are needed.     

Effects of ursodeoxycholic acid and／or low-calorie diet on steatohepatitis in rats with obesity and hyperlipidemia

AIM: To evaluate the effects of ursodeoxycholic acid (UDCA) and/or low-calorie diet (LCD) on a rat model of nonalcoholic steatohepatitis (NASH). METHODS: Fifty-five Sprague-Dawley rats were divided into five groups. The control group (n = 9) was fed with standard rat diet for 12 wk, NASH group (n = 10) was fed with high-fat diet consisted of normal diet, 10% lard oil and 2% cholesterol for 12 wk, UDCA group (n = 10) was fed with high-fat diet supplemented with UDCA at a dose of 25 mg/(kg · d) in drinking water for 12 wk, LCD group (n = 10) was fed with high-fat diet for 10 wk and then LCD for 2 wk, and UDCA+LCD group (n = 15) was fed with high-fat diet for 10 wk, followed by LCD+UDCA for 2 wk. At the end of the experiment, body weight, serum biochemical index, and hepatopathologic changes were examined. RESULTS: Compared with the control group, rats in the NASH group had significantly increased body weight, liver weight, and serum lipid and aminotransferase levels. All rats in the NASH group developed steatohepatitis, as determined by their liver histology. Compared with the NASH group, there were no significant changes in body weight, liver weight, blood biochemical index, the degree of hepatic steatosis, and histological activity index (HAI) score in the UDCA group; however, body and liver weights were significantly decreased, and the degree of steatosis was markedly improved in rats of both the LCD group and the UDCA+LCD group, but significant improvement with regard to serum lipid variables and hepatic inflammatory changes were seen only in rats of the UDCA+LCD group, and not in the LCD group. CONCLUSION: LCD might play a role in the treatment of obesity and hepatic steatosis in rats, but it exerts no significant effect on both serum lipid disorders and hepatic inflammatory changes. UDCA may enhance the therapeutic effects of LCD on steatohepatitis accompanied by obesity and hyperlipidemia. However, UDCA alone is not effective in the prevention of steatohepatitis induced by high-fat diet.     

Plasma leptin is influenced by diet composition and exercise

OBJECTIVE: A low-fat, high-carbohydrate diet (相似文献   

Effects of diet and exercise on adipocytokine levels in patients with moderate to severe chronic kidney disease

Background and aimsObesity is a pro-inflammatory risk factor for progression of CKD and cardiovascular disease. We hypothesized that implementation of caloric restriction and endurance exercise would improve adipocytokine profiles in patients with moderate to severe CKD.Methods and resultsWe enrolled patients with moderate to severe CKD through a multi-center pilot randomized trial of diet and exercise in a 4-arm design (dietary restriction of 10%–15% reduction in caloric intake, exercise three times/week, combined diet and exercise, and control) (NCT01150851). Adipocytokines (adiponectin and leptin) were measured at the beginning and end of the study period as secondary outcomes. Treatment effect was analyzed in a multivariable model adjusted for baseline outcome values, age, gender, site and diabetes. A total of 122 participants were consented, 111 were randomized (42% female, 25% diabetic, and 91% hypertensive), 104 started intervention and 92 completed the study (Figure 1). Plasma adiponectin levels increased significantly in response to diet by 23% (95% CI: 0.2%, 49.8%, p = 0.048) among participants randomized to the caloric restriction and usual activity arm but not to exercise, whereas circulating leptin did not change by either treatment.ConclusionOur data suggest that dietary caloric restriction increases plasma adiponectin levels in stage 3–4 CKD patients, with limited effect on leptin levels. These findings suggest the potential for improving the metabolic milieu of CKD with moderate calorie restriction.     

肥胖患者瘦素水平与冠心病的相关性研究

目的：探讨肥胖患者瘦素水平与冠心病的关系。方法：选取2018年9月~2019年10月广西医科大学第一附属医院心内科收治的胸痛查因（未有冠心病史）择期做冠状动脉造影的肥胖患者（BMI≥27 kg/㎡）作为研究对象,根据冠脉造影结果将患者分为冠心病组和对照组,对两组进行性别、年龄1：1匹配后,剩下46对作为最终研究对象。结果：在多元线性回归分析显示,瘦素与性别（女性,R2=0.495, β=0.385, P＜0.001）、高密度脂蛋白（R2=0.495, β=0.034, P=0.014）有独立的正向相关性。多变量二元Logistic回归分析显示,血清瘦素水平与冠心病独立相关（OR=2.363,95%CI：1.234-4.524,P=0.009）;当瘦素水平作为分类变量进行分析时,最高三分位数的冠心病风险是最低三分位数的3.865倍（P=0.048）。结论：在肥胖人群中,瘦素水平升高与冠心病独立相关。     

Effects of low-calorie diet on steatohepatitis in rats with obesity and hyperlipidemia

AIM: To evaluate the effects of low calorie diet (LCD) on nonalcoholic steatohepatitis (NASH) in rats with obesity and hyperlipidemia.METHODS: 29 Sprague-Dawley (SD) rats were randomly divided into three groups. The animals in control (n=9) and NASH group (n=10) were fed on standard rat diet and high fat diet respectively for 12 weeks, ten rats in LCD group were fed on high fat diet for 10 weeks and then low calorie diet for 2 weeks. At the end of the experiment, body weight, abdominal adipose content, liver function, and hepatopathological changes were examined to evaluate the effect of different feeding protocols on the experimental animals.RESULTS: There was no death of animal in the experimental period. All rats in the NASH group developed steatohepatitis according to liver histological findings. Compared with the control group, body weight (423.5±65.2 vs 351.1±43.0 g,P＜0.05), abdominal adipose content (14.25±1.86 vs9.54±1.43,P＜0.05), liver index (3.784-±0.533 vs2.957±±0.301%, P＜0.01),total serum cholesterol (1.60±0.41 vs 1.27±0.17 mmol/L, P＜0.05)and free fatty acids (728.2±178.5 vs 429.2±96.7 mmol/L,P＜0.01), serum alanine aminotransferase (1 257.51±671.34vs671.34±118.57 nkat/L, P＜0.05) and aspartic aminotransferse (2 760.51±998.66 vs 1 648.29±414.16 nkat/L, P＜0.01) were significantly increased in the NASH group. Whereas, when rats were fed on LCD protocol, their body weight (329.5±38.4 g,P＜0.01), abdominal adipose content (310.21±1.52 g, P＜0.05),liver index (3.199±0.552 %, P＜0.05), and serum alanine aminotransferase (683.03±245.49 nkat/L, P＜0.05) were significantly decreased, and the degree of hepatic steatosis (P＜0.05) was markedly improved compared with those in the NASH group. However, no significant difference was found in serum lipid variables and hepatic inflammatory changes between the two groups.CONCLUSION: LCD might play a role in the prevention and treatment of obesity and hepatic steatosis in SD rats,but it exerts no significant effects on both serum lipid disorders and hepatic inflammatory changes.     

The effect of short-term exercise on plasma leptin levels in patients with anorexia nervosa

Plasma leptin concentrations are markedly reduced in malnourished patients with anorexia nervosa (AN). Whether the long-term underweight and low-fat stores affect the leptin response to exercise remains unknown. We investigated the effect of 45-minute cycle ergometer exercise (2 W kg-1 of lean body mass [LBM]) on plasma leptin, norepinephrine (NE), glycerol, and insulin levels in 10 patients with AN and in 15 healthy age-matched women (C). Plasma leptin levels immediately and 90 minutes after the exercise bout were significantly reduced compared with basal leptin levels in both AN and C groups (P<.05). Compared with the control trial, leptin levels were significantly lower immediately and 90 minutes after exercise in the AN group (P<.05) but not in the C group. Basal and exercise-induced plasma glycerol and NE levels did not differ significantly between the groups. Basal and exercise-induced plasma insulin levels were significantly lower in the AN group compared with the C group (P<.05). In conclusion, we demonstrated that a single bout of low-intensity exercise significantly reduces plasma leptin levels in patients with AN. In healthy women, exercise had no effect on lowering leptin concentrations beyond the diurnal decrease that occurs in the absence of exercise. Neither NE nor insulin are responsible for the different response of leptin to exercise in AN.     

Leptin resistance - or why leptin fails to work in obesity.

In experimental models of obesity high serum concentrations of leptin without subsequent inhibition of food intake indicate a resistance to the physiological effects of leptin. Similar to the animal model leptin concentrations in most of the obese patients are higher compared to normal-weight persons. The postulated leptin resistance is one major target in the search for a better understanding of obesity and the development of pharmacological tools to treat this spreading disease.     

An alpha1-receptor blocker reduces plasma leptin levels in hypertensive patients with obesity and hyperleptinemia.

Obesity is often complicated by hypertension, and both conditions are risk factors for atherosclerosis. Leptin has attracted attention as a possible cause of hypertension in obese persons. We investigated the effect of a slow-release alpha1-receptor blocker, bunazosin hydrochloride, on leptin levels and insulin resistance in obese hypertensive patients with hyperleptinemia. The subjects were 17 patients (12 men and 5 women aged 56.1 +/- 12.2 years) with essential hypertension who were not receiving alpha1-receptor blockers. They had a body mass index (BMI) > or = 25 kg/m2 and a plasma leptin concentration > or = 5 ng/ml. They received oral therapy with bunazosin hydrochloride at doses of up to 9 mg/day. The plasma leptin concentration, body weight, blood pressure, heart rate, fasting blood glucose, plasma insulin concentration, and free fatty acid level were compared between before and after treatment. Although there was no significant change of BMI, there was a significant decrease of plasma leptin after treatment (10.6 +/- 5.4 ng/ml vs. 8.7 +/- 3.4 ng/ml, p = 0.0128), as well as a significant decrease of plasma insulin (9.8 +/- 4.8 microU/ml vs. 8.1 +/- 4.6 microU/ml, p = 0.0494) and HOMA-R (2.9 +/- 2.1 vs. 2.2 +/- 1.5, p = 0.0237). In conclusion, bunazosin hydrochloride reduced the plasma leptin level and improved insulin resistance in hypertensive patients with obesity and hyperleptinemia.     

Relationship between the changes of plasma levels of leptin and obesity in patients with insulinoma

<正>Objective To analyze the relationship between the changes of fasting plasma level of leptin and obesity in patients with insulinoma before operation.Methods From January 2003 to May 2008,40 patients with insulinoma diagnosed at Peking Union Medical College Hospi-     

腹内型肥胖的代谢特点及合并NIDDM后的变化

应用核磁共振（ＭＲＩ）测量１６例肥胖者，１０例肥胖伴ＮＩＤＤＭ者，及８例正常体重者的腹部皮下、腹内及股部脂肪，观察体脂含量及分布对糖、脂、胰岛素代谢的影响。结果表明：肥胖对糖、脂、胰岛素代谢异常的影响尤以腹内肥胖组为显著，总体脂增加与葡萄糖及游离脂肪酸关系密切；腹内脂肪增加对胰岛素分泌和代谢影响较为显著，胰岛素的清除尚与股部脂肪有关；腹部脂肪与股部脂肪比值是体脂分布对糖、脂、胰岛素代谢影响的较重要     

Recombinant methionyl human leptin administration to achieve high physiologic or pharmacologic leptin levels does not alter circulating inflammatory marker levels in humans with leptin sufficiency or excess

A role for high leptin levels in the proinflammatory state associated with obesity has been proposed on the basis of observational studies, but a recent interventional study employing administration of long-acting pegylated leptin resulting in very high pharmacologic levels in obese subjects did not support this idea. These interventional studies have not yet been independently confirmed, however, and varying levels and duration of hyperleptinemia as well as the presence of comorbidities such as diabetes have not yet been investigated as potential effect modifiers. We performed three interventional studies involving administration of recombinant methionyl human leptin (r-metHuLeptin) to lean, otherwise healthy obese, and obese diabetic subjects to investigate whether increasing circulating leptin levels over a wide spectrum of values (from low physiologic to high pharmacologic) would alter serum levels of inflammatory markers and other cytokines important in the T helper cell response. Increasing leptin levels from low physiologic to high physiologic in lean men and from higher physiologic to low pharmacologic in obese men over 3 d did not alter serum interferon-gamma, IL-10, TNF-alpha, monocyte chemoattractant protein-1, or soluble intercellular adhesion molecule-1. In obese subjects with type 2 diabetes mellitus, the administration of r-metHuLeptin for 4 or 16 wk, resulting in high pharmacologic leptin levels, did not activate the TNF-alpha system or increase cytokines or inflammatory markers, including IL-10, IL-6, C-reactive protein, monocyte chemoattractant protein-1, and soluble intercellular adhesion molecule-1. These findings do not support an etiopathogenic role for leptin in proinflammatory states associated with leptin excess such as obesity and have direct relevance for the potential future therapeutic use of r-metHuLeptin in humans.     

Two-month effects of individualized exercise training with or without caloric restriction on plasma adipocytokine levels in obese female adolescents

Objectives

To examine if, in young obese patients, an individualized training programme in association with a caloric restriction programme which had an effect on whole-body lipid oxidation, was able to induce changes on plasma adipocytokine concentrations.

Materials and methods

Twenty-seven obese female adolescents participated in the study. Whole-body lipid oxidation during exercise was assessed by indirect calorimetry during a graded cycle ergometer test. Body mass (BM), body mass index (BMI), percentage of body fat (%BF), insulin homeostasis model assessment (HOMA-IR) and fasting levels of circulating adipocytokines were assessed prior and after a two-month diet programme, individualized training programme targeted at Lipox_max corresponded to the power at which the highest rate of lipids was oxidized and combined diet/training programme.

Results

The diet/training programme induced both a shift to a higher-power intensity of Lipox_max (+27.8 ± 5.1 W; p < 0.01) and an increase of lipid oxidation at Lipox_max (+96.8 ± 16.2 mg/min; p < 0.01). The enhancement in lipid oxidation was significantly (p < 0.01) correlated with the diet/training-induced improvement in %BF (r = −0.47), HOMA-IR (r = −0.66), leptin (r = −0.41), TNF-α (r = −0.48), IL-6 (r = −0.38), adiponectin (r = 0.43) and resistin (r = 0.51).

Conclusion

This study showed that in obese female adolescents a moderate training protocol targeted at Lipox_max and combined with a diet programme improved their ability to oxidize lipids during exercise, and that this improvement was associated with changes in plasma adipocytokine concentrations.     

Association of leptin levels with obesity and blood pressure: possible common genetic variation

OBJECTIVE: To ascertain the extent to which relationships between obesity (OB) and blood pressure (BP) can be explained by an individual's leptin plasma levels. DESIGN: Pedigree-based cross-sectional study in an apparently healthy population of European origin. SUBJECTS: The study sample is comprised of 90 nuclear and more complex families totaling 210 male and 213 female subjects aged 18-75 y, randomly recruited in Bashkorstan Autonomic region, Russia. MEASUREMENTS: Various fatness and fat distribution traits (including nine circumferences (CRCs), and eight skinfolds (CKFs) by anthropometry), blood pressure, and plasma leptin levels (by ELISA kits). RESULTS: Adjustment for circulating leptin led to attenuation of the magnitude of correlations between OB and BP, regardless of trait pair and sex cohort. Some of these correlations became statistically nonsignificant. All familial effects were gone, and heritability estimates became virtually zero after adjustment of each of the OB traits and systolic blood pressure (SBP) in offspring for leptin values in parents. CONCLUSION: BP and OB covariation is substantially mediated by circulating leptin levels. As a result, body fat has only a weak independent effect on BP variation after adjustment for leptin levels. Our findings also strongly suggest that genetic variation in body mass index, SKFs, and even body CRCs, as well as of SBP is due to genetic variation of leptin. Genetic variation of diastolic blood pressure in the present sample, however, shared very little with that of leptin.     

The effects of exercise on C-reactive protein, insulin, leptin and some cardiometabolic risk factors in Egyptian children with or without metabolic syndrome

ABSTRACT: BACKGROUND: The prevalence and magnitude of obesity in the children and the adolescents have increased dramatically in the developing countries over the last 20-30 years. The prevalence of metabolic syndrome (MS) in children is increasing. Aim: This study aimed to investigate the changes of C-reactive protein (CRP), leptin, insulin, and blood lipids before and after the exercise therapy in normal and obese children (with or without metabolic syndrome). METHODS: The study covered 49 normal children (control), 32 obese children without metabolic syndrome and 12 obese children with metabolic syndrome. We examined the influence of exercise (3 times/week) for 12 weeks on the levels of serum CRP, leptin, insulin, homeostatic model assessment insulin resistance (HOMA-IR), triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDLC) in all groups. RESULTS: There were significant correlations between HOMA-IR and the individual components of the metabolic syndrome. After 12 weeks of exercise, both of the obese children groups, with and without metabolic syndrome, showed reduced body weight, body mass index (BMI), and CRP level, and increased HDL-C level. The percentage of metabolic syndrome decreased from 12.9 % before the exercise training to 7.5 % after training. Also, there was a significant reduction in BMI (from 47.3 to 32.6 %), in systolic blood pressure (from 18.3 to 15.1 %) and in HDL-C level (from 18.3 to 9.7 %). CONCLUSION: Overweight children have multiple risk factors associated with the metabolic syndrome. 12- week exercise may have a positive effect on reducing risk factors for the metabolic syndrome.