Abstract
Leptin is well acknowledged as an anorexigenic hormone that plays an important role in feeding control. Hypothalamic GABA system plays a significant role in leptin regulation on feeding and metabolism control. However, the pharmacological relationship of leptin and GABA receptor is still obscure. Therefore, we investigated the effect of leptin or combined with baclofen on the food intake in fasted mice. We detected the changes in hypothalamic c‐Fos expression, hypothalamic TH, POMC and GAD67 expression, plasma insulin, POMC and GABA levels to demonstrate the mechanisms. We found that leptin inhibit fasting‐induced increased food intake and activated hypothalamic neurons. The inhibitory effect on food intake induced by leptin in fasted mice can be reversed by pretreatment with baclofen. Baclofen reversed leptin's inhibition on c‐Fos expression of PAMM in fasted mice. Therefore, these results indicate that leptin might inhibit fasting‐triggered activation of PVN neurons via presynaptic GABA synaptic functions which might be partially blocked by pharmacological activating GABA‐B. Our findings identify the role of leptin in the regulation of food intake.
Highlights
Feeding behaviour is one of the most basic physiological activities of humans and animals and is closely related to energy expenditure and metabolism
Our result found that 16-hour food deprivation significantly increased the cumulative food intake and the increase was gradually weakened over time as previously reported.[25]
We observed that pretreatment with baclofen reversed leptin-induced reduction of food intake in fasted mice, indicating that gamma-aminobutyric acid (GABA)-B receptor might be implicated in the regulation of food intake by leptin
Summary
Feeding behaviour is one of the most basic physiological activities of humans and animals and is closely related to energy expenditure and metabolism. It is well acknowledged that acute or chronic fasting can trigger overeating and hyperphagia.[1] In the past decades, leptin, a hormone encoded by ob gene and secreted by adipose cells, is well studied in energy balance and glucose metabolism.[2,3] A number of animal studies have shown that leptin can suppress appetite and reduce the food consumption via acting on specific neurons in hypothalamus.[4]. We further demonstrate the potential molecular mechanisms via investigating hypothalamic neuronal activation, glutamate decarboxylase 67 (GAD67), tyrosine hydroxylase (TH) and POMC protein levels of hypothalamus, serum insulin, POMC and GABA levels alterations after systematic administration of leptin or combined with baclofen
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