Taurine supplementation reduces adiposity and hepatic lipid metabolic activity in adult offspring following maternal cafeteria diet.

Maternal taurine supplementation has been shown to exert protective effects following a maternal obesogenic diet on offspring growth and metabolism. However, the long-term effects of maternal cafeteria diet on adiposity, metabolic profile, and hepatic gene expression patterns following supplementation of taurine in adult offspring remains unclear. In this study, we hypothesized that exposure to maternal taurine supplementation would modulate the effects of maternal cafeteria diet by reducing adiposity and hepatic gene expression patterns involved in lipid metabolism in adult offspring. Female Wistar rats were fed a control diet, control diet supplemented with 1.5% taurine in drinking water, cafeteria diet (CAF) or CAF supplemented with taurine (CAFT) from weaning. After 8 weeks, all animals were mated and maintained on the same diets during pregnancy and lactation. After weaning, all offspring were fed with control chow diet until the age of 20 weeks. Despite similar body weights, CAFT offspring had significantly lower fat deposition and body fat when compared with CAF offspring. Microarray analysis revealed that genes (Akr1c3, Cyp7a1, Hsd17b6, Cd36, Acsm3, and Aldh1b1) related to steroid hormone biosynthesis, cholesterol metabolism, peroxisome proliferator-activated receptor signaling pathway, butanoate metabolism, and fatty acid degradation were down-regulated in CAFT offspring. The current study shows that exposure to maternal cafeteria diet promoted adiposity and taurine supplementation reduced lipid deposition and in both male and female offspring and led to alterations in hepatic gene expression patterns, reducing the detrimental effects of maternal cafeteria diet.

From a toxin to an obesogen: a review of potential obesogenic roles of acrylamide with a mechanistic approach.

Obesity and obesity-related disorders such as cancer, type 2 diabetes, and fatty liver have become a global health problem. It is well known that the primary cause of obesity is positive energy balance. In addition, obesity is the consequence of complex gene and environment interactions that result in excess calorie intake being stored as fat. However, it has been revealed that there are other factors contributing to the worsening of obesity. The presence of nontraditional risk factors, such as environmental endocrine-disrupting chemicals, has recently been associated with obesity and comorbidities caused by obesity. The aim of this review was to examine the evidence and potential mechanisms for acrylamide having endocrine-disrupting properties contributing to obesity and obesity-related comorbidities. Recent studies have suggested that exposure to environmental endocrine-disrupting obesogens may be a risk factor contributing to the current obesity epidemic, and that one of these obesogens is acrylamide, an environmental and industrial compound produced by food processing, particularly the processing of foods such as potato chips, and coffee. In addition to the known harmful effects of acrylamide in humans and experimental animals, such as neurotoxicity, genotoxicity, and carcinogenicity, acrylamide also has an obesogenic effect. It has been shown in the literature to a limited extent that acrylamide may disrupt energy metabolism, lipid metabolism, adipogenesis, adipocyte differentiation, and various signaling pathways, and may exacerbate the disturbances in metabolic and biochemical parameters observed as a result of obesity. Acrylamide exerts its main potential obesogenic effects through body weight increase, worsening of the levels of obesity-related blood biomarkers, and induction of adipocyte differentiation and adipogenesis. Additional mechanisms may be discovered. Further experimental studies and prospective cohorts are needed, both to supplement existing knowledge about acrylamide and its effects, and to clarify its established relationship with obesity and its comorbidities.

Cafeteria diet increased adiposity in comparison to high fat diet in young male rats.

BACKGROUND: Dietary intervention studies in animal models of obesity are crucial to elucidate the mechanistic effects of specific nutrients and diets. Although several models of diet induced obesity have been examined in rodents to assess obesity, there are few studies that have researched influence of different high fat and/or westernized diets. The aim of this study was to compare a high fat diet and a cafeteria diet on obesity related biochemical and physiological parameters in young male rats. METHODS: Five week old Wistar male rats were fed a control chow diet (C), butter-based high fat diet (HF) or cafeteria diet (CAF) for twelve weeks. In HF, 40% of energy came from fat and this ratio was 46% in CAF. CAF composed of highly energetic and palatable human foods along with chow diet. At the end of the feeding protocol all animals were culled using CO2 asphyxia and cervical dislocation after an overnight fasting. RESULTS: Total energy and fat intake of CAF was significantly higher than C and HF. CAF was more effective in inducing obesity, as demonstrated by increased weight gain, Lee index, fat depot weights and total body fat in comparison to C and HF. Despite increased adiposity in CAF, plasma glucose, insulin and HOMA-IR levels were similar between the groups. Plasma leptin and cholesterol levels were markedly higher in CAF than C and HF. DISCUSSION: We have demonstrated that there are differential effects of high fat diet and cafeteria diet upon obesity and obesity-related parameters, with CAF leading to a more pronounced adiposity in comparison to high fat diet in young male rats. Future studies should consider the varied outcomes of different diet induced obesity models and development of a standardized approach in similar research practices.