Obesity is a leading risk factor for insulin resistance, hypertension, hyperlipidemia, and cardiovascular complications, collectively referred to as metabolic diseases. Given the prevalence of obesity and its associated medical problems, new strategies are required to prevent or treat obesity and obesity-related metabolic effects. Here we summarize contributors of obesity, and molecular mechanisms controlling adipogenesis from studies in mammalian systems. We also discuss the possibilities of using Drosophila as a genetic model system to advance our understanding of players in fat biology.
Animals ; Drosophila/*physiology ; Humans ; Metabolic Syndrome X/*etiology/metabolism/prevention & control ; Obesity/*complications/metabolism/prevention & control ; PPAR gamma/metabolism/physiology

Obesity worldwide is constantly increasing. Obesity acts as an independent significant risk factor for malignant tumors of various organs including colorectal cancer. Visceral adipose tissue is physiologically more important than subcutaneous adipose tissue. The relative risk of colorectal cancer of obese patients is about 1.5 times higher than the normal-weight individuals, and obesity is also associated with premalignant colorectal adenoma. The colorectal cancer incidence of obese patients has gender-specific and site-specific characteristics that it is higher in men than women and in the colon than rectum. Obesity acts as a risk factor of colorectal carcinogenesis by several mechanisms. Isulin, insulin-like growth factor, leptin, adiponectin, microbiome, and cytokines of chronic inflammation etc. have been understood as its potential mechanisms. In addition, obesity in patients with colorectal cancer negatively affects the disease progression and response of chemotherapy. Although the evidence is not clear yet, there are some reports that weight loss as well as life-modification such as dietary change and physical activity can reduce the risk of colorectal cancer. It is very important knowledge in the point that obesity is a potentially modifiable risk factor that can alter the incidence and outcome of the colorectal cancer.
Adipokines/metabolism/physiology ; Body Mass Index ; Colorectal Neoplasms/*etiology/prevention & control ; Energy Intake ; Exercise ; Humans ; Insulin Resistance ; Meta-Analysis as Topic ; Obesity/*complications ; Somatomedins/metabolism/physiology ; Weight Loss

Adolescent ; Adult ; Aged ; Body Fat Distribution ; Body Mass Index ; Diabetes Mellitus, Type 2 ; complications ; Fatty Liver ; etiology ; pathology ; prevention & control ; Female ; Humans ; Intra-Abdominal Fat ; metabolism ; pathology ; Male ; Middle Aged ; Obesity ; complications ; Risk Factors ; Severity of Illness Index ; Young Adult

OBJECTIVETo study the effect of rosiglitazone on serum high-sensitivity C-reactive protein (hs-CRP), interleukin-1beta (IL-1beta), IL-6, tumor necrosis factor-alpha (TNF-alpha) and insulin resistance in obese patients with newly diagnosed type 2 diabetes.

METHODSThis study involved 118 patients with newly diagnosed type 2 diabetes and obesity, who were randomly assigned into two groups for a 12-week treatment with rosiglitazone (4 mg/day, group A) or sulfonylureas (group B). Serum hs-CRP, IL-1beta, IL-6, TNF-alpha, fasting plasma glucose (FPG) and fasting insulin (FINS) were measured before and after the treatment. Insulin resistance index was calculated according to the HOMA Model.

RESULTSIn group A, rosiglitazone treatment resulted in significantly reduced serum hs-CRP, IL-1beta, IL-6, TNF-alpha, FPG and insulin resistance index (P<0.01). No difference in FPG was found between the two groups after the treatment (P>0.05), but serum hs-CRP, IL-1beta, IL-6, TNF-alpha and insulin resistance index were significantly lower in group A than in group B (P<0.05).

CONCLUSIONRosiglitazone can decrease FPG, reduce the inflammation reaction and improve insulin resistance in obese patients with type 2 diabetes.

Adult ; Aged ; Aged, 80 and over ; C-Reactive Protein ; metabolism ; Diabetes Mellitus, Type 2 ; blood ; complications ; drug therapy ; Female ; Humans ; Hypoglycemic Agents ; therapeutic use ; Inflammation ; blood ; prevention & control ; Insulin Resistance ; Interleukin-1beta ; blood ; Interleukin-6 ; blood ; Male ; Middle Aged ; Obesity ; complications ; Thiazolidinediones ; therapeutic use ; Tumor Necrosis Factor-alpha ; blood

OBJECTIVETo investigate the therapeutic effects of Ping-tang Recipe (, PTR) on high-fat diet (HFD)-induced insulin resistance and non-alcoholic fatty liver disease (NAFLD), and to elucidate the underlying mechanisms.

METHODSForty male SD rats were included in the study. Ten rats were fed on normal diet as normal control, and thirty rats were fed on HFD for 8 weeks to induce obesity, followed with low dose (0.42 g/kg) or high dose (0.84 g/kg) of PTR or vehicle for 8 weeks with 10 animals for each group. Glucose metabolism and insulin sensitivity were evaluated by oral glucose tolerance test and insulin tolerance test. Hepatic steatosis was measured by immunohistochemistry. Liver lipid metabolic genes were analyzed by quantitative real-time polymerase chain reaction, while AMP-activated protein kinase (AMPK) expression was examined by Western blot.

RESULTSRats fed on HFD developed abdominal obesity, insulin resistance and NAFLD. PTR treatment reduced visceral fat (peri-epididymal and peri-renal) accumulation, improved glucose metabolism, and attenuated hepatic steatosis. The expressions of the key lipolytic regulating genes, including peroxisome proliferators-activated receptor γ co-activator 1α (PGC-1α), peroxisome proliferator-activated receptor γ (PRAR-γ) and α (PRAR-α), were up-regulated (P<0.05 or P<0.01), while the expressions of lipogenic genes such as sterol regulatory element-binding protein 1c (SREBP-1c), fatty acid synthase (FAS) and liver fatty acid-binding protein (L-FABP) were down-regulated (P<0.05 or P<0.01). In addition, PTR activated AMPK and promoted acetyl-CoA carboxylase phosphorylation in the liver.

CONCLUSIONSPTR improves insulin resistance and reverse hepatic steatosis in the rat model of HFD-induced obesity through promotion of lipolysis and reduction of lipogenesis, which involves the AMPK signaling pathway, thus representing a new therapeutic intervention for obesity related insulin resistance and NAFLD.

AMP-Activated Protein Kinases ; metabolism ; Animals ; Body Weight ; drug effects ; Diet, High-Fat ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Fatty Liver ; blood ; complications ; prevention & control ; Gene Expression Regulation ; drug effects ; Glucose ; metabolism ; Glucose Tolerance Test ; Insulin Resistance ; Intra-Abdominal Fat ; drug effects ; pathology ; Lipogenesis ; drug effects ; Lipolysis ; drug effects ; Liver ; drug effects ; enzymology ; pathology ; Male ; Obesity ; blood ; complications ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Triglycerides ; metabolism