| Popis: |
Poor dietary choices are the largest modifiable risk factor contributing to the rising epidemic of obesity and related metabolic diseases. This effect can span generations, both through the continued physical environment and imprinted parental effects on offspring. The glycaemic index (GI) is a measure of carbohydrate quality based on its effect on alterations in blood glucose levels over time, with low GI diets being widely reported to improve metabolic health, both in humans and rodents. Studies that aim to investigate the effect of a high versus low GI diet often do so by adding resistant starch to the low GI diet, which, as a type of fibre, possesses GI-independent positive metabolic effects, clouding the delineation of mechanisms underlying low GI health benefits. A systematic review and meta-analysis of high GI rodent diets confirmed both the overall positive effect of low GI diets, and the lack of studies utilizing well-controlled diets, particularly in terms of resistant starch. Rodent diets that differed only in the base sugar carbohydrate were constructed to control for fibre content, but differ in GI, as confirmed through meal tests in mice modelled after the clinical standard. To examine the effect of maternal dietary GI on offspring metabolic programming, these diets were utilised in a generational study in C57BL/6 mice, with dams and pups metabolically examined via EchoMRI, Promethion™ metabolic cages and oral glucose tolerance tests. Glucose-fed dams and pups were larger and fatter, while sucrose and fructose-fed dams had increased insulin responses and liver triglyceride due to excess dietary fructose. The low GI isomaltulose-based diet also caused unexpected consequences on foetal development, female pup adiposity and pup insulin response. While the high-sugar diets were not as obesogenic as high-fat diets, compared with chow-fed controls representing whole, unprocessed foods, there was evidence of programming greater adiposity in female offspring. |
