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Fig. 1 | Nutrition & Metabolism

Fig. 1

From: Chronic stress, epigenetics, and adipose tissue metabolism in the obese state

Fig. 1

Endocrine disruptions in the obese state. Increased fat mass in obesity results in greater secretion of leptin from adipose tissue, while the expression of leptin receptor and transport of leptin across the blood–brain barrier (BBB) are reduced, leading to lowered leptin signaling and eventually leptin resistance. Sequentially, kisspeptin, which is modulated by leptin, is lowered, leading to hypogonadism in obese males and hyperandrogenism in obese females through the regulation of the hypothalamic-pituitary–gonadal (HPG) axis. Meanwhile, expansion of β-cell mass in the obese state is associated with increased production of insulin, which is further exacerbated by leptin resistance, leading to hyperinsulinemia. Hyperinsulinemia also contributes to the disturbance in sex hormones in obese males and females, which eventually promotes food intake while inhibiting lipid mobilization. Increased food intake inhibits the secretion of ghrelin, resulting in decreased production of growth hormone (GH) and reduced lipid mobilization. Moreover, an increase in fat mass in the obese state promotes the release of thyroid-stimulating hormone (TSH), which then increases the activation of triiodothyronine (T3) via the hypothalamic-pituitary-thyroid (HPT) axis, while the expression of TSH receptor is lowered in the obese state, leading to reduced negative feedback and more release of free TSH and T3 into the circulation. These events lead to thyroid dysfunction and reduced energy expenditure which eventually contribute to fat mass accretion. Finally, obesity is associated with increased production of cortisol and hyperactivation of the hypothalamic–pituitary–adrenal (HPA) axis, which abnormally modulates stress responses later on, thereby influencing food intake and in turn fat mass

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