Abstract
Previous studies have shown that Ginkgo biloba extract (GbE) reduces food intake and body mass gain and regulates proteins related to lipid metabolism in obese rats. In ovariectomized rats, GbE restored the hippocampal and hypothalamic serotonergic system activity, favoring the spontaneous feeding decrement. Considering the promising hypophagic effect of GbE, this study aimed to investigate the effect of a single acute dose on hypothalamic pathways that regulate feeding behavior in male rats. Four-month-old Wistar male rats received either a single acute oral GbE dose (500 mg/kg) or vehicle. Food intake and body mass were measured after 1, 4, 12, and 24 h. Rats were euthanized, and hypothalami were removed for mRNA quantification of anorexigenic (POMC/CART) and orexigenic (AgRP/NPY) neuropeptides, leptin/serotonin receptors (5HT1A, 5HT1B, 5HT2C), and serotonin transporters. We also investigated POMC, 5-HT1B, and 5-HT2C protein levels. A single acute GbE dose induced the hypothalamic POMC, CART, and 5-HT2C gene expression but failed to modify orexigenic effectors. No alterations in food intake, body mass, and hypothalamic protein levels were observed. In summary, the present findings demonstrate the rapid stimulation of pivotal hypothalamic anorexigenic pathways in response to a single GbE administration, reinforcing the GbE hypophagic activity. However, more studies are necessary to evaluate its potential as an appetite modulator.
Highlights
The regulation of energy homeostasis and feeding behavior are mainly performed by the hypothalamus, a central area responsible for the integration of peripheral and neural signals regarding feeding and body energy status [1]
We have previously reported that Ginkgo biloba extract (GbE) supplementation for 14 days reduced food intake, body mass gain, and visceral adiposity in diet-induced obese male rats (DIO) [15,16,17]
Since important anorexigenic and anti-obesogenic effects were observed after a prolonged supplementation with GbE in different animal models, the present study aimed to investigate the initial sequence of events related to the anorexigenic effects of GbE
Summary
The regulation of energy homeostasis and feeding behavior are mainly performed by the hypothalamus, a central area responsible for the integration of peripheral and neural signals regarding feeding and body energy status [1]. Some important hypothalamic mediators of energy homeostasis are the neuropeptide Y (NPY) and agouti-related peptide (AgRP) orexigenic effectors, while the proopiomelanocortin (POMC) and cocaine and amphetamine-regulated transcript (CART) are recognized as pivotal anorexigenic effectors [3] Peripheral hormones, such as the adipokine leptin, and the pancreatic hormone insulin inform the hypothalamus about the long-term energy status to reduce the activity of orexigenic pathways and stimulate the anorexigenic signaling [1,4,5]. It is well established that, during a meal, the extracellular hypothalamic serotonin levels raise in order to promote satiation, and interrupting the acute food intake [6,7] This hypophagic response associated with the serotonin activity is mainly related to the stimulation of POMC/CART neurons by the activation of the 5-HT2C receptor [8]. Heisler and colleagues [10] demonstrated that the activation of the 5-HT1B receptor inhibited
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