Metformin is an antidiabetic drug used for the treatment of diabetes and metabolic diseases. Imbalance in the autonomic nervous system (ANS) is associated with metabolic diseases. This study aimed to test whether metformin could improve ANS function in obese rats.
View Article and Find Full Text PDFIt is known that antidiabetic drug metformin, which is used worldwide, has anti-cancer effects and can be used to prevent cancer growth. We tested the hypothesis that tumor cell growth can be inhibited by early treatment with metformin. For this purpose, adult rats chronically treated with metformin in adolescence or in adulthood were inoculated with Walker 256 carcinoma cells.
View Article and Find Full Text PDFIntroduction: A sedentary lifestyle and high-fat feeding are risk factors for cardiometabolic disorders. This study determined whether moderate exercise training prevents the cardiometabolic changes induced by a high-fat diet (HFD).
Materials And Methods: Sixty-day-old rats were subjected to moderate exercise three times a week for 30 days.
Background/aims: The objective of the current work was to test the effect of metformin on the tumor growth in rats with metabolic syndrome.
Methods: We obtained pre-diabetic hyperinsulinemic rats by neonatal treatment with monosodium L-glutamate (MSG), which were chronically treated every day, from weaning to 100 day old, with dose of metformin (250 mg/kg body weight). After the end of metformin treatment, the control and MSG rats, treated or untreated with metformin, were grafted with Walker 256 carcinoma cells.
Background: Postnatal early overfeeding and physical inactivity are serious risk factors for obesity. Physical activity enhances energy expenditure and consumes fat stocks, thereby decreasing body weight (bw). This study aimed to examine whether low-intensity and moderate exercise training in different post-weaning stages of life is capable of modulating the autonomic nervous system (ANS) activity and inhibiting perinatal overfeeding-induced obesity in rats.
View Article and Find Full Text PDFBackground/aims: Impaired pancreatic beta cell function and insulin secretion/action are a link between obesity and type 2 diabetes, which are worldwide public health burdens. We aimed to characterize the muscarinic acetylcholine receptor (mAChR) M1-M4 subtypes in isolated pancreatic islets from pre-diabetic obese rats that had been treated neonatally with monosodium L-glutamate (MSG).
Methods: At 90 days of age, both the MSG and the control groups underwent biometric and biochemical evaluation.
Nutritional insults during developmental plasticity have been linked with metabolic diseases such as diabetes in adulthood. We aimed to investigate whether a low-protein (LP) diet at the beginning of adulthood is able to program metabolic disruptions in rats. While control rats ate a normal-protein (23%; NP group) diet, treated rats were fed a LP (4%; LP group) diet from 60 to 90 days of age, after which an NP diet was supplied until they were 150 days old.
View Article and Find Full Text PDFBackground/aims: Brown adipose tissue activation has been considered a potential anti-obesity mechanism because it is able to expend energy through thermogenesis. In contrast, white adipose tissue stores energy, contributing to obesity. We investigated whether the early programming of obesity by overfeeding during lactation changes structure of interscapular brown adipose tissue in adulthood and its effects on thermogenesis.
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