Marcela Barthichoto

Voluntary running decreases nonexercise activity in lean and diet-induced obese mice.

PURPOSE Determine whether voluntary wheel running triggers compensatory changes in nonexercise activity in lean and high-fat diet fed mice. METHODS C57Bl/6 mice received a control (C) or a high-fat diet (H) and half of them had free access to a running wheel 5days/week (CE and HE, respectively) for 10weeks. Energy intake, nonexercise activity (global activity, distance covered and average speed of displacement in the home cage) and energy expenditure (EE) were evaluated at weeks 5 and 10 during the 2days without the wheels. RESULTS High-fat diet increased weight gain in H (110%) and HE (60%) groups compared to C and CE groups, respectively, with no effect of exercise. Wheel running increased energy intake (26% CE, 11% HE in week 5; 7% CE, 45% HE in week 10) and decreased distance covered (26% for both CE and HE in week 5; 35% CE and 13% HE in week 10) and average speed (35% CE and 13% HE in week 5; 45% CE and 18% HE in week 10) compared to the respective nonexercised groups. In week 10 there was an interaction between diet and exercise for global activity, which was reduced nearly 18% in CE, H, and HE groups compared to C. Access to a running wheel increased EE in week 5 (11% CE and 16% HE) but not in week 10, which is consistent with the period of highest running (number of turns: weeks 1-5 nearly 100%>weeks 6-10 for CE and HE groups). EE was reduced in H (19%) and HE (12%) groups compared to C and CE, in week 10. CONCLUSION Voluntary running causes a compensatory decrease in nonexercise activity and an increase in energy intake, both contributing to the lack of effect of exercise on body mass.

The effects of calorie-matched high-fat diet consumption on spontaneous physical activity and development of obesity

Aims: To characterize the effects of a calorie matched high‐fat diet (HFD) on spontaneous physical activity (SPA), body weight, inflammatory status and expression of genes related to energy homeostasis in hypothalamus of mice. Main methods: C57Bl/6 mice (n = 5 per group) were fed a control diet (16.5% calories from fat) ‐ control group (C), or a calorie matched HFD (60% calories from fat). We evaluated, periodically, body weight and SPA by infrared beam sensors and, at the end of the 12th week, we verified blood glucose levels, fat pads weight, plasma insulin, TNF‐&agr; and IL‐6 by ELISA and the hypothalamic expression of 84 genes related to energy homeostasis, by quantitative real‐time PCR array. Key findings: Isocaloric HFD reduced SPA already in the first 48 h and SPA was kept lower in the HFD compared to C throughout. These changes resulted in an increase in body weight, adiposity, TNF‐&agr; and IL‐6, blood glucose and hyperinsulinemia in the HFD group when compared to the C group. Expression of the Agrp, Bdnf, Adra2b and Pyy genes were altered in the hypothalamus of HFD‐fed mice, highlighting the downregulation of Bdnf, key regulator of energy homeostasis. Significance: Dietary macronutrient distribution plays an important part in energy homeostasis that goes beyond its energy content. Despite calorie‐matched, the HFD led to increased body weight and adiposity due to decreased SPA, highlighting the key role of SPA on energy balance. The changes in hypothalamic gene expression seem to underlie the reduction in SPA caused by HFD.

Spontaneous physical activity and mediators of energy homeostasis in the hypothalamus of mice from 4 to 10 months of age

What is the central question of this study? Is the initial decline of spontaneous physical activity (SPA) in mice related to impaired insulin and leptin signalling or brain‐derived neurotrophic factor expression in the hypothalamus? What is the main finding and its importance? We showed that SPA started to decline at an early stage, concomitantly with an impairment of hypothalamic leptin signalling. Consequently, energy expenditure decreased and glucose tolerance worsened. Our results demonstrate the need to counteract the initial decline in SPA to avoid metabolic impairments and indicate the possible involvement of central leptin in the reduction in SPA with age.