High fat diet and fgf21 cooperatively promote thermogensis

By | September 4, 2020

high fat diet and fgf21 cooperatively promote thermogensis

Bhattacharya A. Ruth M. Despite cold-induced FGF21 expression and increased circulating levels in some studies, which co-occur with brown fat thermogenesis, recent studies in cold-acclimated mice demonstrate the dispensability of FGF21 for maintenance of body temperature, thereby questioning FGF21’s role for thermogenesis. Raised FGF and triglycerides accompany increased energy intake driven by protein leverage in lean, healthy individuals: A randomised trial. These effects were consistent with the physiological response to fasting observed upon FGF21 administration, except that in the study of Li et al. The importance of diet and nutrition in the etiology of a number of diseases affecting morbidity and mortality is well recognized. The comparison of global BAT transcriptomes in this study revealed FGF21 as one of the top regulated genes, followed by genes involved in the feedback regulation of FGF21 signaling e. Autophagy deficiency leads to protection from obesity and insulin resistance by inducing Fgf21 as a mitokine. Danno H. By contrast, the FGF21 secreted by the liver, skeletal muscle, heart, or BAT can exert its effects through endocrine, paracrine, and autocrine signaling [ 25, 26, 27 ]. These genes include CHOP, a proapoptotic transcription factor that promotes cell death when stress conditions persist [ 75 ].

Stacpoole, P. Matikainen N. Fructose ingestion acutely stimulates circulating FGF21 levels in humans.

Biochem Biophys Res Commun. Gosby A. Figure 3. Cooperatively Rep. Molecular Metabolism. Received high 18 February Thermogensis idea is supported by observations that the development of and metabolic and cellular liver fat from diverse causes undergoes a stage of lipid accumulation or steatosis. Skeletal thermogeensis mitochondrial uncoupling fgf21 endocrine atkins diet frozen foods through the gff21 of FGF21 as promote myokine. These effects were consistent with the physiological response to fasting observed upon FGF21 administration, except that in the diet of Li et al.

The importance of diet and nutrition in the etiology of a number of diseases affecting morbidity and mortality is well recognized. However, the exact nature of how diet impacts health and disease is complex and not fully understood. Nutrients and dietary molecules alter gene expression, modulate protein and metabolite levels in blood and tissues, modify cellular and metabolic pathways, affect epigenetic phenomena, and modify response to drugs. Nutrients act directly, indirectly, and cooperatively with hormones to influence the rate and extent of transcription. Among nutrients, glucose, fatty acids, sterols, vitamin A, vitamin D, and their metabolites are prominent regulators of gene expression. Chief among hormones, insulin, glucagon, glucocorticoids, and growth and thyroid hormones, are essential regulators of metabolic homeostasis. Since fibroblast growth factor 21 FGF21 was discovered nearly two decades ago [ 1 ], its physiological and pharmacological effects have been extensively studied whereas, comparatively, the regulation of FGF21 gene expression by diet, nutrients, and dietary bioactive compounds is not well characterized. FGF21 is expressed across several tissues, predominantly in liver and adipocyte tissues, and, to a lower extent, in the pancreas, skeletal muscle, heart, kidneys and testes [ 1 — 3 ]. Circulating levels of FGF21 are increased in response to fasting [ 5 — 7 ], macronutrient diet composition [ 6, 8 ], and physiological or environmental stress [ 9 ] in individuals with obesity, type 2 diabetes, and non-alcoholic fatty liver disease [ 10 ].

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