Effects of intermittent fasting and chronic swimming exercise on body composition and lipid metabolism.

Intermittent fasting protocol (IFP) has been suggested as a strategy to change body metabolism and improve health. The effects of IFP seem to be similar to aerobic exercise, having a hormetic adaptation according to intensity and frequency. However, the effects of combining both interventions are still unknown. Therefore, the aim of the present study was to evaluate the effects of IFP with and without endurance-exercise training on body composition, food behavior, and lipid metabolism. Twenty-week-old Wistar rats were kept under an inverted circadian cycle of 12 h with water ad libitum and assigned to 4 different groups: control group (ad libitum feeding and sedentary), exercise group (ad libitum feeding and endurance training), intermittent fasting group (IF; intermittent fasting and sedentary), and intermittent fasting and exercise group (IFEX; intermittent fasting and endurance training). After 6 weeks, the body weight of IF and IFEX animals decreased without changes in food consumption. Yet, the body composition between the 2 groups was different, with the IFEX animals containing higher total protein and lower total fat content than the IF animals. The IFEX group also showed increases in total high-density lipoprotein cholesterol and increased intramuscular lipid content. The amount of brown adipose tissue was higher in IF and IFEX groups; however, the IFEX group showed higher expression levels of uncoupling protein 1 in this tissue, indicating a greater thermogenesis. The IFP combined with endurance training is an efficient method for decreasing body mass and altering fat metabolism, without inflicting losses in protein content.

SOCS3 expression within leptin receptor-expressing cells regulates food intake and leptin sensitivity but does not affect weight gain in pregnant mice consuming a high-fat diet.

Pregnancy induces transitory metabolic changes including increases in food intake and body fat deposition, as well as leptin and insulin resistance. Recent findings have suggested that increased hypothalamic expression of suppressor of cytokine signaling-3 (SOCS3) is a key mechanism responsible for triggering those metabolic adaptations. Because obesity is a risk factor for gestational metabolic imbalances, we aimed to study the role of SOCS3 during pregnancy in obese mice. Female mice carrying a deletion of SOCS3 in leptin receptor-expressing cells (SOCS3 KO mice) were exposed to a chronic high-fat diet (HFD), and we then studied their energy balance and glucose homeostasis during pregnancy. SOCS3 deletion did not prevent diet-induced obesity or changes in body weight and adiposity observed during pregnancy. However, the typical increase in food intake during mid- and late-pregnancy was blunted in SOCS3 KO females. We also observed a slight improvement in glucose homeostasis and increased leptin sensitivity in the arcuate nucleus of the hypothalamus in pregnant SOCS3 KO mice on HFD. Despite this, SOCS3 KO mice had an increased number of uterine reabsorptions and fewer fetuses compared to the controls. Compared to control animals, a reduction in proopiomelanocortin and an increase in oxytocin mRNA levels were observed in the hypothalamus of pregnant SOCS3 KO mice. In contrast to previous studies using lean animals, conditional SOCS3 ablation did not prevent major gestational metabolic changes in diet-induced obese mice. Our findings contribute to the understanding of the role of SOCS3 in mediating pregnancy-induced metabolic adaptations.