ro13-9904 and Insulin-Resistance

This study aimed to explore whether exposure to ceftriaxone during early life could influences glucose and lipid metabolism of high fat diet-induced mice.. Total 48 of female BALB/c aged 2 week old were randomly divided into control group(treated with saline), antibiotic group(treated with100 mg/kg ceftriaxone), high-fat diet group(treated with saline) and combined action group(treated with 100 mg/kg ceftriaxone)(n=12), respectively to stop gavage 2 weeks later. Then high-fat diet group and combined action group were fed with high-fat diet for 12 weeks. Fasting blood glucose(FBG) and oral glucose tolerance test were conducted in the last week. Serum total cholesterol(TC), triglyceride(TG), high-density lipoprotein cholesterol(HDL-C), low-density lipoprotein cholesterol(LDL-C), fasting insulin, leptin and TG, TC in liver were also measured. Furthermore, homeostasis model assessment of insulin resistance(HOMA-IR) was calculated from FBG and insulin.. Compared with normal chow diet, high-fat diet impaired oral glucose tolerance and increased the levels of abdominal adipose tissue, FBG, HOMA-IR, lips in serum and liver and leptin(P<0. 05). The oral administration of ceftriaxone in early life impaired oral glucose tolerance and increased the levels of abdominal adipose tissue, FBG and TG in liver(P<0. 05). In addition, early ceftriaxone intervention could enhance the impaired glucose tolerance, the increasing FBG, insulin resistance and liver lipids associated with high-fat diet(P<0. 05).. Early ceftriaxone intervention not only significantly increases the level of abdominal adipose tissue, FBG, insulin resistance and liver lipids, but also enhances glycolipid metabolic disorders induced by high-fat diet. These result suggest that the exposure to antibiotics in the early life might increase the sensitivity of host animal to high fat diet induced abnormal glycolipid metabolism late.

Topics: Administration, Oral; Animals; Blood Glucose; Ceftriaxone; Diet, High-Fat; Female; Glycolipids; Insulin; Insulin Resistance; Lipid Metabolism; Mice; Mice, Inbred BALB C; Random Allocation