OBJECTIVETo study the effects of Jiaotai Pill (JTP) and its single components on ectopic fat accumulation in rats with type 2 diabetes mellitus (T2DM).

METHODSThe T2DM model of rat was established by injection of streptozotocin from tail vein and high fat-caloric diet feeding. Model rats were randomly divided into the model group and four treated groups were treated respectively with JTP and its single components, Rhizoma Coptidis, Cinnamon and metformin, via gastric perfusion. Meanwhile, a normal control group was also set up. Body weight (BW), liver index (LI), levels of fasting plasma glucose (FPG), fasting serum insulin (FINS) and insulin resistance index (HOMA-IR), plasma activities of liver associated enzymes (LAE), triglyceride (TG) contents and pathological changes of liver, heart and muscle were determined before and after a 8-week treatment.

RESULTSAs compared with the normal rats, BW, LI, LAE activities, HOMA-IR, TG contents of the liver, heart and muscle were all increased in the model rats (P<0.05 or P<0.01), with pathologic appearance of fatty degeneration in different degrees. Compared with the model group, LI, LAE, HOMA-IR, and TG contents in the liver, heart and muscle tissues were decreased in different extents in the four treated groups (P<0.05 or P<0.01), and the histology of tissues in them was restored to near normal. Compared with the metformin treated group, the hepatic and muscular TG contents decreased in the JTP treated group (P<0.01), and the muscular TG content in the Rhizoma Coptidis treated group were lower (P<0.05). And the gamma-GT level in the JTP treated group was the lowest in the three Chinese drugs treated groups (P<0.01).

CONCLUSIONSThe disturbances of glucose and lipid metabolism and abnormality of liver function in T2DM rats could be improved by JTP and its single components. The mechanism might be related to their effects in improving insulin resistance and reducing ectopic fat accumulation.

Adiposity ; drug effects ; Animals ; Diabetes Mellitus, Experimental ; drug therapy ; Diabetes Mellitus, Type 2 ; drug therapy ; Drugs, Chinese Herbal ; therapeutic use ; Insulin Resistance ; Intra-Abdominal Fat ; pathology ; Lipid Metabolism ; drug effects ; Liver ; pathology ; Male ; Muscle, Skeletal ; metabolism ; Phytotherapy ; Rats ; Rats, Wistar

OBJECTIVETo investigate the effects of Liuweidihuang pills (LP) on visceral fat deposition in Otsuka Long-Evans Tokushima Fatty (OLETF) rats.

METHODSForty male OLETF rats were randomly divided into LP group and control group (n=20 per group), and 10 male Long-evans Tokushima Otsuka (LETO) rats were used as normal controls. The rats in LP group were given LP(2.4 mg/kg) daily by intragastric administration since the age of 8 weeks, and those in the other two groups were given water of the same volume by intragastric administration. Blood glucose of all the rats was determined by oral glucose tolerance test (OGTT) and visceral fat deposition examined after the rats were sacrificed.

RESULTSOLETF rats had obviously greater amount of visceral fat than LETO rats (P<0.05) and administration of LP ameliorated the increment of visceral fat deposition in this type 2 diabetic model, producing significant effect at the age of 40 weeks (P<0.01).

CONCLUSIONLP may effectively decrease visceral fat deposition in OLETF rats.

Animals ; Blood Glucose ; metabolism ; Diabetes Mellitus, Type 2 ; blood ; drug therapy ; pathology ; Drugs, Chinese Herbal ; therapeutic use ; Intra-Abdominal Fat ; drug effects ; pathology ; Male ; Obesity ; pathology ; prevention & control ; Phytotherapy ; Random Allocation ; Rats ; Rats, Inbred OLETF

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

OBJECTIVETo investigate the antiobesity effect of Jueming Prescription (JMP), a Chinese herbal medicine formula, and its influence on mRNA expressions of beta3 adrenergic receptor (beta3-AR) and uncoupling protein-2 (UCP-2) in adipose tissue of diet-induced obese rats.

METHODSFifty male Sprague-Dawley rats were randomly divided into the normal control group (n =8) that was on a standard chow diet, and the obese model group (n =42) that was on a diet of high fat chow. Two weeks after the high fat diet, 29 obese rats in the obese model group were further randomly divided into 3 groups: the untreated obese model group (n =9), the metformin group (n =10, metformin 300 mg kg⁻¹ day)⁻¹, and the JMP group (n =10, JMP 4 g kg⁻¹ day⁻¹). After 8-week treatment, body weight, wet weight of visceral fat, and percentage of body fat (PBF) were measured. The levels of fasting blood glucose, serum lipids, and insulin were assessed, and insulin sensitivity index (ISI) was calculated. The adipose tissue section was stained with hematoxylin-Eosin, and the cellular diameter and quantity of adipocytes were evaluated by light microscopy. The mRNA expressions of beta3-AR and UCP-2 from the peri-renal fat tissue were determined by real-time reverse transcription polymerase chain reaction (RT-PCR).

RESULTSCompared with the obese model group, treatment with JMP resulted in significantly lower body weight, wet weight of visceral fat, PBF, and diameter of adipocytes, and significantly higher level of high-density lipoprotein cholesterol, ISI (all P<0.01), JMP increased the mRNA expressions of beta3-AR and UCP-2 from perirenal fat tissue (P <0.05, P<0.01).

CONCLUSIONSJMP could reduce body weight and adipocyte size; and the effect was associated with the up-regulation of beta3-AR and UCP-2 expressions in the adipose tissue and improvement of insulin sensitivity.

Adipocytes ; drug effects ; metabolism ; pathology ; Adiposity ; drug effects ; Animals ; Blood Glucose ; metabolism ; Body Weight ; drug effects ; Cell Size ; drug effects ; Diet, High-Fat ; Drugs, Chinese Herbal ; pharmacology ; Epididymis ; drug effects ; pathology ; Fasting ; blood ; Gene Expression Regulation ; drug effects ; Insulin ; blood ; Intra-Abdominal Fat ; drug effects ; metabolism ; pathology ; Ion Channels ; genetics ; metabolism ; Lipids ; blood ; Male ; Mitochondrial Proteins ; genetics ; metabolism ; Obesity ; blood ; genetics ; pathology ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, beta-3 ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Uncoupling Protein 2 ; Weight Loss ; drug effects

This study was conducted to evaluate whether the composition of carbohydrate or fat diet affects insulin resistance by measuring the muscle glucose transport rate. Both high-sucrose and high-starch diet with or without high-fat decreased insulin-stimulated glucose transport, but there were no significant differences among groups. Calorie intake in both high-sucrose and high-starch diet groups was higher than in chow group. The high-fat high-sucrose diet induced decrease in insulin-stimulated glucose transport was partially improved by supplement with fish oil. Calorie intake in high-fat high-sucrose and fish oil supplemented groups was higher than in chow group. The decreased insulin-stimulated glucose transport was accompanied by the increase in visceral fat mass, plasma triglyceride and insulin levels. These changes were improved by the supplement with fish oil. These results demonstrate that the composition of fat in diet is clearly instrumental in the induction of muscle insulin resistance. However, in high carbohydrate diet, it is likely that the amount of calorie intake may be a more important factor in causing insulin resistance than the composition of carbohydrate. Thus, the compositions of carbohydrate and fat in diet differentially affect on muscle insulin resistance.
Animals ; Blood Glucose/metabolism ; Body Weight ; Diet ; Dietary Carbohydrates/*pharmacology ; Dietary Fats/*pharmacology ; Dietary Supplements ; Energy Intake/drug effects ; Fish Oils/pharmacology ; Insulin/blood ; Insulin Resistance/*physiology ; Intra-Abdominal Fat/drug effects/metabolism ; Male ; Muscle, Skeletal/*drug effects/physiology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo explore the effects of soy isoflavone (SIF) on low-grade inflammation in rats with high-fat diet-induced insulin resistance (IR) and explore the mechanisms of SIF in improving insulin sensitivity.

METHODSThe rats with high-fat diet-induced IR were randomly divided into one model control group and 3 SIF groups gavaged with SIF water solutions at the doses of 50, 150, and 450 mg/kg, respectively. One month after the treatment, fasting blood glucose (FBG), fasting insulin (FINS), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), C-reactive protein (CRP), resistin and adiponectin in the serum were detected by enzymatic method, radioimmunoassay, or enzyme-linked immunosorbent assay.

RESULTSIn the 150 and 450 mg/kg SIF groups, fasting body-weights, visceral adipose tissue deposition, FINS, resistin, TNF-alpha in serum, and IR index were lowered in comparison with the model control group, and in 450 mg/kg SIF group, serum IL-6 level was obviously lowered, and adiponectin increased. No differences were found in serum C-reactive protein levels between the 3 SIF groups.

CONCLUSIONSoy isoflavone may ameliorate insulin sensitivity by decreasing visceral adipose deposition and adjusting low-grade inflammatory molecules derived from white adipose tissue.

Adiponectin ; blood ; Animals ; Body Weight ; drug effects ; C-Reactive Protein ; metabolism ; Inflammation ; blood ; physiopathology ; Insulin ; blood ; Insulin Resistance ; Interleukin-6 ; blood ; Intra-Abdominal Fat ; drug effects ; metabolism ; Isoflavones ; pharmacology ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Resistin ; blood ; Soybeans ; chemistry ; Tumor Necrosis Factor-alpha ; blood