Abstract:
:The obesity is a result of energy imbalance and the increase in thermogenesis seems an interesting alternative for the treatment of this disease. The mechanism of energy expenditure through thermogenesis is tightly articulated in the hypothalamus by leptin. The hypothalamic extracellular signal-regulated kinase-1/2 (ERK1/2) is a key mediator of the thermoregulatory effect of leptin and mediates the sympathetic signal to the brown adipose tissue (BAT). In this context, physical exercise is one of the main interventions for the treatment of obesity. Thus, this study aimed to verify the effects of acute physical exercise on leptin-induced hypothalamic ERK1/2 phosphorylation and thermogenesis in obese mice. Here we showed that acute physical exercise reduced the fasting glucose of obese mice and increased leptin-induced hypothalamic p-ERK1/2 and uncoupling protein 1 (UCP1) content in BAT ( P < 0.05). These molecular changes are accompanied by an increased oxygen uptake (VO 2 ) and heat production in obese exercised mice ( P < 0.05). The increased energy expenditure in the obese exercised animals occurred independently of changes in spontaneous activity. Thus, this is the first study demonstrating that acute physical exercise can increase leptin-induced hypothalamic ERK1/2 phosphorylation and energy expenditure of obese mice.
journal_name
J Cell Biochemjournal_title
Journal of cellular biochemistryauthors
Gaspar RC,Muñoz VR,Kuga GK,Nakandakari SCBR,Minuzzi LG,Botezelli JD,da Silva ASR,Cintra DE,de Moura LP,Ropelle ER,Pauli JRdoi
10.1002/jcb.27426subject
Has Abstractpub_date
2019-01-01 00:00:00pages
697-704issue
1eissn
0730-2312issn
1097-4644journal_volume
120pub_type
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