Appetite control

Abstract

Our understanding of the physiological systems that regulate food intake and body weight has increased immensely over the past decade. Brain centres, including the hypothalamus, brainstem and reward centres, signal via neuropeptides which regulate energy homeostasis. Insulin and hormones synthesized by adipose tissue reflect the long-term nutritional status of the body and are able to influence these circuits. Circulating gut hormones modulate these pathways acutely and result in appetite stimulation or satiety effects. This review discusses central neuronal networks and peripheral signals which contribute energy homeostasis, and how a loss of the homeostatic process may result in obesity. It also considers future therapeutic targets for the treatment of obesity.

Association of Obesity with Serum Leptin, Adiponectin, and Serotonin and Gut Microflora in Beagle Dogs

“…After induction of obesity, the plasma 5HT levels were markedly decreased in the obese group. Experimentally induced obesity is known to decrease 5HT levels 44. Inflammation associated with changes in the gut microbiota is considered to decrease 5HT availability during obesity 43, 45.…”

To subjugate NPY is to improve the quality of life and live longer

“…NPY expressing neurons in the arcuate nucleus (ARC), dorsomedial hypothalamus (DMH) and brain stem (BS) innervate various hypothalamic sites implicated in integration of energy balance (30,36,39,40,64). These NPY neurons also coexpress various neurotransmitters.…”

“…synthesis in ARC perikarya, storage and release in the terminal field in the ARC-PVN axis) showed the episodic rise and fall in NPY release to be temporally correlated with initiation and termination of the appetitive drive (36,39,40). Knowledge of this tight temporal relationship between neurosecretion and behavior greatly assisted in delineating the precise roles of afferent hormonal signals from the periphery, such as leptin from white adipose tissue (WAT), ghrelin and peptide YY (PYY 3 -36) from gastrointestinal tract and insulin from pancreas β-cells, in the release of NPY antecedent to meal initiation (3,4,8,22,35,42,44,52,53,55,60,64,65). Photoperiodic cues and the time of food availability also interact in modulating the periodic antecedent NPY neurosecretion in the ARC-PVN axis (36,39,40,55,60,65).…”

“…NPY expressing neurons in the DMH and BS are goaded into action to cope with those physiological and environmental challenges that demand increased energy, such as lactation or derangements in afferent neural and hormonal feedback signals to the hypothalamus (36,(39)(40)(41). In addition, the hypothalamic NPY network exerts control on the hypothalamic anorexigenic melanocortin and the orexigenic orexin and melanin concentrating hormone (MCH) signaling to NPY Y 1 and Y 5 receptor expressing targets in the ARC-PVN axis (2,30,36,39,40,64).…”

“…Since the demonstration of the potent appetite stimulating effects of neuropeptide Y (NPY) and cohorts in 1984 (18), these signaling molecules have been at the forefront of the intense research directed toward deciphering the dialogue between peripheral signals and hypothalamic circuits that orchestrate ingestive behavior in mammals (8,30,36,39,40,64). In addition to a pivotal role in hypothalamic integration of energy homeostasis, the hypothalamic NPY network has since been shown to play a role in neuroendocrine control of reproduction and lactation, fluid balance, growth, stress, temperature, general body metabolism and bone health (1,12,15,31,41,45,46,48,62).…”