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Genetics of Energy Intake and Food Preferences
Published in Claude Bouchard, The Genetics of Obesity, 2020
Louis Pérusse, Claude Bouchard
It is generally believed that both genetic and environmental factors influence the mechanisms controlling appetite and satiety.27 As shown in Table 4, several peptides are known to alter feeding behavior, either by stimulating or inhibiting food intake.28 It has been suggested that cholecystokinin and neuropeptide Y are two peptides that best fit a series of criteria to qualify as regulators of eating behavior.29 These peptides, and undoubtedly others, therefore represent potential candidate genes for the study of the impact of genetic variation in food intake and eating behavior. The expression of the neuropeptide Y gene has been shown to be increased in genetically obese animals, an observation which suggests that genes may indeed contribute to the development of disturbed eating behavior and obesity.30 Moreover, it is also becoming evident that some of the peptides known to stimulate or inhibit food intake are acting specifically on some nutrients such as fat or carbohydrate.28
Neurohumoral Regulation
Published in Thomas F. Lüscher, Paul M. Vanhoutte, The Endothelium: Modulator of Cardiovascular Function, 2020
Thomas F. Lüscher, Paul M. Vanhoutte
Neuropeptide Y is stored in certain adrenergic nerve endings together with norepinephrine.281 The peptide evokes contraction of most isolated blood vessels. In the canine coronary artery and in small arteries of human skeletal muscle, the effects of the peptide do not involve the endothelium.966 In contrast, in the ear artery of the rabbit the augmentation of adrenergically induced contractions by neuropeptide Y is endothelium dependent.221
The Production of Biologically Active Peptides in Brain Tissues
Published in Gerard O’Cuinn, Metabolism of Brain Peptides, 2020
Somatostatin-14 and somatostatin-28 are derived from prosomatostatin in a manner similar to that of the synthesis of the gastrin molecules. The pro-somatostatin gene is under the regulation of cyclic AMP responsive elements.47 The transcription of genes for proTRH, proCRF and proLHRH are responsive to transcriptional factors that interact with products formed by proto-oncogenes c-fos and c-jun.48–50 There has been a report that the expression of neuropeptide Y, in rat hypothalamus, is responsive to physiological variations in insulin.51
High-fat diet attenuates morphine withdrawal effects on sensory-evoked locus coeruleus norepinephrine neural activity in male obese rats
Published in Nutritional Neuroscience, 2022
Xinyi Li, Chung-Yang Yeh, Nicholas T. Bello
Both clinical and rodent studies have attributed the LC in the stress response, and this could serve as one possible explanation for the involvement of LC in obesity and opioid withdrawal [30,31]. Rodent study has previously shown stress to increase LC activity. Upon stress termination, LC activity return to baseline, but this LC inhibition was absent after infusion of opioid antagonist naloxone, suggesting endogenous opioids play a significant role in counterbalancing the stress effect [32]. Furthermore, the LC has been shown to activate the hypothalamic-pituitary axis (HPA) by disinhibiting the inhibitory effects of medial prefrontal cortex on the paraventricular nucleus [33]. Therefore, the absence of the antagonistic effect of opioid on stress-induced LC activity and the effects of morphine withdrawal in eliciting LC hyperactivity act in concert to promote the stress response. Previous work has shown bingeing of sweetened fats or consumption of palatable food attenuated stress response during restraint stress [17,34]. One possible point of convergence between obesity and stress may lie in neuropeptide Y (NPY), which is a neuropeptide that possesses both anxiolytic and food stimulation properties [35]. Together, these findings suggest HFD to elicit protection against morphine withdrawal-induced stress.
The role of neuropeptide Y, orexin-A, and ghrelin in differentiating unipolar and bipolar depression: a preliminary study
Published in Nordic Journal of Psychiatry, 2022
Mehmet Ünler, İrem Ekmekçi Ertek, Nigar Afandiyeva, Mustafa Kavutçu, Nevzat Yüksel
Neuropeptide Y (NPY) is involved in many physiological functions such as stress response, circadian rhythms, eating behavior, sexual behavior, memory, and blood pressure control [24,25]. Studies on the association between MDD and NPY levels have yielded inconclusive results. While some studies found that MDD patients had lower NPY levels than HCs [26,27], a few studies found no significant correlation between MDD and NPY levels [28,29]. A study with 120 BD patients evaluating the association between suicide risk and NPY levels found significantly lower NPY levels in those with a previous history of suicide. In addition, the patients with lower NPY levels had a significantly higher risk of attempting suicide during the 1-year follow-up. It suggests that NPY levels may be a possible predictor of prospective suicide [30].
Mechanistically acting anti-obesity compositions/formulations of natural origin: a patent review (2010–2021)
Published in Expert Opinion on Therapeutic Patents, 2022
Pracheta Sengupta, Niyati Tiwari, Tanya Bhatt, Atish T. Paul
The nucleus of the hypothalamus can also be directly influenced by circulating factors as it is partially outside the blood–brain barrier. There are two well-characterized neuronal populations involved in this pathway, namely, appetite inhibiting and appetite-stimulating neurons. The appetite inhibiting neurons further includes proopiomelanocortin (POMC) & cocaine and amphetamine-regulated transcript (CART) co-expressing neurons. Appetite-stimulating neurons includes neuropeptide Y (NPY) and agouti-related peptide co-expressing neurons [24–26]. One of the major genes associated with anorexigenic signaling is the melanocortin receptor genes (MC2R, MC3R, and MC4R) that stimulates melanocortin stimulating hormone (MSH) and melanin-concentrating hormone (MCH) [27]. In the hypothalamus, the neurotransmitter α-melanocyte stimulating hormone (α-MSH) is produced that act on the melanocortin receptor in another part of the hypothalamus to reduce food intake. Lack of leptin on the leptin receptor, in both animals and humans, leads to obesity (Figure 1(C)).