5/24/2023 0 Comments Gene construction kit 4.03In reciprocal crossings of A y/a x a/a and a/a x A y/a, a/a and A y/a offspring are born in a 1:1 ratio, which makes it possible to assess the effect of maternal obesity per se on the metabolic phenotype of offspring with a normal metabolism ( a/a). Heterozygous A y/a C57Bl mice have yellow coat color and develop obesity and non-insulin-dependent diabetes with age due to ectopic expression of the agouti gene in the hypothalamus, which evokes chronic blockage of melanocortin receptors (MCRs) by the agouti protein. In mice, the mutation Lethal yellow at the agouti locus ( A y) causes ectopic overexpression of the agouti gene. In order to reveal the programming effect of metabolic changes caused directly by maternal obesity, not by diet, it is possible to use genetic models of obesity that develop when consuming a standard diet. It is not known whether maternal obesity per se influences the offspring’s taste preferences, whether it increases the ability to develop obesity in offspring, and to what extent these maternal influences depend on the sex of the offspring. However, in order to develop methods for correction of offspring early development, it is necessary to understand the programming effect of maternal obesity itself, even when the mother consumes a balanced, healthy diet. In this kind of research, it is difficult to separate the programming influence of maternal diet from the influence of those metabolic disorders in mothers that are directly caused by obesity. Most of the current research on developmental programming is based on laboratory models of diet-induced obesity caused by the consumption of high-calorie diets of various compositions. Therefore, when obese mothers consume a balanced diet, MO does not affect food choice and development of diet-induced obesity in offspring. ![]() In offspring of both sexes, MO had no effect on food choice and metabolic response to SFD intake. SFD consumption caused obesity development and insulin resistance, increased liver expression of glycolytic and lipogenesis genes, and affected hypothalamic expression of anorexigenic and orexigenic genes. MO increased food intake and liver expression of lipogenesis genes in male offspring consuming the SD. ![]() Compared to control mothers, pregnant obese mothers had higher levels of insulin, leptin, and FGF21. Metabolic response to the consumption of a sweet–fat diet (SFD: SD, lard, and sweet biscuits) and the choice of components of this diet were evaluated in their male and female offspring. Metabolic parameters were assessed in pregnant and lactating A y/a (obesity) and a/a (control) mothers. Mice with the Lethal yellow mutation ( A y/a) develop obesity consuming an SD. We evaluated the influence of MO on food choice and susceptibility to obesity in offspring when mothers consumed a standard diet (SD). Maternal diet and obesity (MO) may influence taste preferences and increase the susceptibility to obesity in offspring, but the impact of MO per se to these influences is poorly understood.
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