| Objective:The Doha D theory suggested that malnutrition in early life has a relationship with metabolic disease in later life.Epidemiological studies have indicated that people suffering from famine in early life and overnutrition in adulthood as a result of rapid economic growth may have an increased risk for diabetes and liver steatosis,It is common in country like china which experience famine and rapid economic growth.Although animal studies have indicated that the feast after famine model embodies a disproportionately higher rate of body fat mass recovery than lean mass recovery and an elevated plasma insulin level,the mechanisms by which the feast after famine model leads to these chronic diseases remain unknown.So we set up a famine and catch-up growth rat model to study the mechanism between this strike and insulin resistance,the lipid metabolic change in liver and adipose tissue.Materials and Methods: 4 weeks-aged female Sprague-Dawley(S rats were divided into 6 groups: age-control low-fat group(A),age-control high-fat group,famine low-fat group(,famine high-fat group(,weigh-control low-fat group(E)and weigh-control high-fat group(F).In the first 4 weeks we fed C group and D group rat on 50% amount food as the rat with same weight eat every day.Then we feed C group rat on low-fat food and D group rat on high-fat food.The age-control group rat have the same age with C and D group.The weigh-control group rat have the same weight in the first refeeding days with the C and D group.After we set up this model,we test the plasma glucose,plasma insulin HOMA-IR and IPITT to study the change in insulin resistance.Besides,we study the glucose utilization in muscle and adipose tissue in this model.By these experiments we explore the mechanism by which famine and catch-up growth cause these metabolic change.Results:(1)Compared with weigh-control low-fat group(E),famine low-fat group(showed the same body weight growth.Compared with weigh-control high-fat group(F),famine high-fat group(also showed the same body weight growth.There is no significant change bewteen these six groups in plasma glucose.(2)Compared with the other five groups,famine high-fat group(show a significant increased growth in blood insulin,HOMA-IR and IPITT.Besides,the area of lipid in HE stain of liver tissue and oil red O stain of adipose tissue in famine and high-fat group(is higher than the other five groups.(3)Compared with other five groups,the glucose uptake in muscle and adipose tissue in famine high-fat group(is significant lower than the other five group.However,the glucose uptake in adipose in famine low-fat group is higher than the other five groups.The gene expression of GLUT4 in mesentery adipose in famine and high-fat group(D)is significantly lower than the other five groups.Conclusions: The famine and over-nutrition “double strike”increase rats’ insulin resistance and cause liver and adipose tissue lipid accumulation.As a result of“double strike”,the glucose uptake in muscle and adipose tissue decreased because of lower gene expression of GLUT4.As muscle and adipose uptake less glucose,rats show increased insulin resistance.Then it contribute to liver and adipose lipid accumulation. |