Insulin resistance and subsequent insulin secretory defect are two main features of type 2 diabetes and associated metabolic disorders. The animal models of type 2 diabetes are very complex and are as heterogeneous as the disease. We have evaluated the effect of various antidiabetic and lipid lowering agents (fenofibrate, rosiglitazone, glimepiride, metformin and simvastatin) on the metabolic abnormalities induced by combining a high-fat diet and multiple low-dose streptozocin (MLDS) in mice. Male Swiss albino mice were orally treated with the above agents and fed with a diet containing high fat for 28 days. On day 15 the animals were injected intraperitoneally with low-dose streptozocin (40 mg kg(-1)), which was administered for five consecutive days. At the end of the 28-day treatment plasma metabolic parameters (glucose, triglyceride and immunoreactive insulin) were estimated. The antidiabetic and hypolipidaemic agents exhibited differential effects on these metabolic parameters. With the exception of fenofibrate all these agents reduced the plasma glucose levels, and the effects of metformin and rosiglitazone on glucose were found to be statistically significant. Although the effect of the test drugs on cholesterol was modest, a significant decrease in triglyceride levels was observed with sub-chronic treatment with these agents. Interestingly, glimepiride mildly elevated the insulin levels while the other antidiabetics and hypolipidaemics reduced the insulin levels, with metformin and rosiglitazone exhibiting statistically significant effects on insulin. To our knowledge this is the first report on the effect of various peroxisome proliferator-activated receptor modulators and newer antidiabetics on the metabolic effects induced by the combined high-fat diet and MLDS model of type 2 diabetes in Swiss albino mice. The results suggested the complexity of the hyperglycaemia, hyperinsulinaemia and hypertriglyceridaemia induced by the high-fat diet and MLDS mouse model, and their correction by various antidiabetics and antihyperlipidaemics may have involved diverse mechanisms.

The effect of the hydroalcoholic extract of fruits of Myristica fragrans Houtt. (Myristicaceae) was investigated on chlorpromazine-induced glucose and triglyceride elevations in male Swiss albino mice. After 7 days of oral administration, the extract, at doses of 150 and 450 mg=kg, ameliorated the metabolic abnormalities caused by chlorpromazine as evidenced by significant reduction of glucose and triglyceride (TG) levels (maximal effect of 41% and 53% reduction of glucose and TG, respectively, at 450 mg dose, p < 0.01). The standard antidiabetic rosiglitazone at 10 mg significantly (p < 0.01) reduced the TG (63%) and glucose (40%) levels in this model, while the standard antidiabetic glimepiride has exhibited 55% and 16% reduction in TG and glucose, respectively. In rats fed a high-cholesterol diet, Myristica fragrans extract significantly reduced the elevated TG (47% reduction at 450 mg, p < 0.01) and cholesterol (66.7% reduction at 450 mg, p < 0.01), and also exhibited a reduction in hepatic TG secretion after tyloxapol administration. These data suggest that Myristica fragrans extract ameliorates hyperglycemia and abnormal lipid metabolism in animal models.

To investigate the antinociceptive potential of eugenol on different pain models Bharati Vidyapeeth Deemed in mice. University, Poona College of Pharmacy, Materials and Methods: Eugenol was evaluated (1-100 mg/kg, i.p.) in various Pune 411 038. experimentally induced pain models like, formalin induced hyperalgesia, acetic acid *Present Address: Discovery induced abdominal constrictions, and thermal pain experiment using Eddy's hot plate. Biology, Advinus Therapeutics, Results: Eugenol significantly inhibited acetic acid induced abdominal constrictions, Bioresearch Centre, with the maximal effect (92.73% inhibition) at 100 mg/kg. In formalin induced paw Pune 411057, licking pain model, eugenol exhibited more pronounced antinociceptive effect in the Maharashtra, India. inflammatory phase than the neurogenic phase (maximal effect was 70.33% and 42.22%, respectively, at 100 mg/kg, i.p). A mild reduction in the pain response latency at 100 Received: 31.3.2006 mg/kg, i.p. dose of eugenol was observed in the hotplate thermal pain studies in mice.