PubMed · 16149586
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Miwa Ryo, Tohru Funahashi. 2005. [Adiponectin].. https://pubmed.ncbi.nlm.nih.gov/16149586/
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Lipoprotein lipase mass in preheparin serum (preheparin LPL mass) is assumed to reflect some of the LPL production in the whole body and insulin sensitivity. While metabolic syndrome is a common underlying condition for cardiovascular diseases, biological marker of this syndrome has not been fully established. To clarify the characteristics of preheparin LPL mass in metabolic syndrome, 362 Japanese subjects were studied to examine the relationship between symptoms of metabolic syndrome and preheparin LPL mass and compare with plasma adiponectin. Furthermore the relation with urinary 8-hydroxydeoxyguanosine (8-OHdG) that reflects oxidative stress to DNA was also studied. Both preheparin LPL mass and plasma adiponectin correlated positively with HDL-cholesterol and negatively with body weight and triglyceride. Only preheparin LPL mass showed a negative correlation with fasting blood glucose and HbA1c. Both mean preheparin LPL mass and plasma adiponectin decreased with an increase in severity of the metabolic syndrome with/without obesity and with/without diabetes. The correlation coefficient between preheparin LPL mass and plasma adiponectin was r=0.562. A negative correlation between preheparin LPL mass and urinary 8-OHdG was observed. These results suggest that low preheparin LPL mass may reflect systemic oxidative stress and also a biomarker of the severity of metabolic syndrome.
OBJECTIVE: We aimed to evaluate the prevalence of metabolic syndrome (MS) in a group of obese children and adolescents in Zhejiang in the south of China, and to compare risk factors such as insulin resistance, adiponectin level and impaired glucose tolerance (IGT) etc with that of simple obese group (SOB) and non-obese healthy group, and also to evaluate the effect of metformin and lifestyle intervention in MS group by up to a 3-month follow-up. METHODS: Three hundred and forty eight moderately or severely obese adolescents aged between 7 and 16 years were enrolled. Oral glucose tolerance test (OGTT), biochemical indicators, blood pressure and body mass index (BMI) were assessed in all of them. Three subgroups were selected (MS group, SOB and healthy control). Adiponectin levels, Whole body insulin sensitive index (WBISI), homeostasis model of insulin resistance (HOMA-IR), plasma lipid and blood pressure were compared in these three groups. Thirty out of thirty-six MS subjects with age over 10 years received metformin treatment combined with lifestyle modification. RESULTS: (1) The prevalence of MS was 10.34% among all obese subjects, which increased with the severity of obesity and reached 22.1% in severely obese children and adolescents. The occurrence of more than one complication reached 72.13%. The incidence of type 2 diabetes and IGT were 1.44 and 1.44% respectively. (2) BMI, waist-to-hip ratio (WHR) and HOMA-IR increased stepwise in the control group, SOB and MS group, whereas serum adiponectin and WBISI decreased stepwise (all P<0.01). Systolic pressure, triglyceride, total cholesterol, low-density lipoprotein cholesterol and postprandial 2-h blood glucose in the MS group increased significantly compared to those in control and SOBs (all P<0.01). A correlation analysis showed that serum levels of adiponectin and WBISI were associated with the components of MS (all P<0.05). (3) After metformin and lifestyle intervention, clinical symptoms were ameliorated, serum adiponectin levels were actually increased and HOMA-IR was dropped in 20/30 MS children who had finished a 3-months follow-up (all P<0.01). CONCLUSION: The prevalence of MS in severely obese children and adolescents in Zhejiang area has reached a high level. Insulin resistance and hypoadiponectinemia were found in these MS children. Metformin combined with lifestyle modification was confirmed to be efficient and safe in treating the obese adolescents with MS.
Leptin and adiponectin, the main metabolic products of adipose tissue, have been implicated in a wide spectrum of human diseases. Given the frequent presence of hepatic steatosis in several chronic liver diseases, there is currently increasing interest in the role of these adipokines in the development of hepatic steatosis and also in necroinflammation and fibrosis, mostly in patients with nonalcoholic fatty liver disease or chronic hepatitis C. According to experimental data, reduced adiponectin levels and increased leptin levels associated with leptin resistance, which are usually observed in obese patients with or without metabolic syndrome, may result in fat accumulation in the liver and in the enhancement of liver inflammation and mostly fibrogenesis. Increased leptin and decreased adiponectin serum levels have been detected initially in patients with nonalcoholic steatohepatitis and more recently in patients with chronic hepatitis C compared to healthy controls in most but not all studies, while the data on the associations between these adipokine levels and the severity of hepatic steatosis or fibrosis are still rather conflicting. However, several potential confounding parameters were not evaluated in all studies. Therefore, the associations between adipokines and liver histological lesions and their effects on liver cells should be evaluated further in prospective, carefully designed studies, including larger cohorts of patients with detailed assessment of metabolic and other potential confounding factors.