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Protective Effects of Melatonin against Obesity-Induced by Leptin Resistance.
Suriagandhi, V, Nachiappan, V
Behavioural brain research. 2022;:113598
Abstract
Consumption of an exceedingly high-fat diet with irregular eating and sleeping habits is typical in the current sedentary lifestyle, leading to chronic diseases like obesity and diabetes mellitus. Leptin is a primary appetite-regulating hormone that binds to its receptors in the hypothalamic cell membrane and regulates downstream appetite-regulating neurons NPY/AgRp and POMC in the hypothalamus. Based on the fat content of the adipose tissue, leptin is secreted, and excess accumulation of fat in adipose tissue stimulates the abnormal secretion of leptin. The secreted leptin circulating in the bloodstream uses its transporters to cross the blood-brain barrier (BBB) and reach the CSF. There is a saturation limit for leptin bound to its transporters to cross the BBB, and increased leptin secretion in adipose tissue has a defect in its transport across the BBB. Leptin resistance is due to excess leptin, a saturation of its transporters, and deficiency in either the receptor level or signalling in the hypothalamus. Leptin resistance leads to obesity due to excess food intake and less energy expenditure. Normal leptin secretion follows a rhythm, and alteration in the lifestyle leads to hormonal imbalances and increases ROS generation leading to oxidative stress. The sleep disturbance causes obesity with increased lipid accumulation in adipose tissue. Melatonin is the master regulator of the sleep-wake cycle secreted by the pineal gland during the night. It is a potent antioxidant with anti-inflammatory properties. Melatonin is secreted in a pattern called the circadian rhythm in humans as well. Research indicates that melatonin plays a vital role in hormonal regulation and energy metabolism, including leptin signalling and secretion. Studying the role of melatonin in leptin regulation will help us combat the pathologies of obesity caused by leptin resistance.
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Appetite, the enteroendocrine system, gastrointestinal disease and obesity.
Crooks, B, Stamataki, NS, McLaughlin, JT
The Proceedings of the Nutrition Society. 2021;(1):50-58
Abstract
The enteroendocrine system is located in the gastrointestinal (GI) tract, and makes up the largest endocrine system in the human body. Despite that, its roles and functions remain incompletely understood. Gut regulatory peptides are the main products of enteroendocrine cells, and play an integral role in the digestion and absorption of nutrients through their effect on intestinal secretions and gut motility. Several peptides, such as cholecystokinin, polypeptide YY and glucagon-like peptide-1, have traditionally been reported to suppress appetite following food intake, so-called satiety hormones. In this review, we propose that, in the healthy individual, this system to regulate appetite does not play a dominant role in normal food intake regulation, and that there is insufficient evidence to wholly link postprandial endogenous gut peptides with appetite-related behaviours. Instead, or additionally, top-down, hedonic drive and neurocognitive factors may have more of an impact on food intake. In GI disease however, supraphysiological levels of these hormones may have more of an impact on appetite regulation as well as contributing to other unpleasant abdominal symptoms, potentially as part of an innate response to injury. Further work is required to better understand the mechanisms involved in appetite control and unlock the therapeutic potential offered by the enteroendocrine system in GI disease and obesity.
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Involvement of Ghrelin Dynamics in Stress-Induced Eating Disorder: Effects of Sex and Aging.
Yamada, C
International journal of molecular sciences. 2021;(21)
Abstract
Stress, a factor that affects appetite in our daily lives, enhances or suppresses appetite and changes palatability. However, so far, the mechanisms underlying the link between stress and eating have not been fully elucidated. Among the peripherally produced appetite-related peptides, ghrelin is the only orexigenic peptide, and abnormalities in the dynamics and reactivity of this peptide are involved in appetite abnormalities in various diseases and psychological states. This review presents an overview of the research results of studies evaluating the effects of various stresses on appetite. The first half of this review describes the relationship between appetite and stress, and the second half describes the relationship between the appetite-promoting peptide ghrelin and stress. The effects of sex differences and aging under stress on appetite are also described.
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4.
Salt need needs investigation.
Leshem, M
The British journal of nutrition. 2020;(11):1312-1320
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Abstract
Expensive and extensive studies on the epidemiology of excessive Na intake and its pathology have been conducted over four decades. The resultant consensus that dietary Na is toxic, as well as the contention that it is less so, ignores the root cause of the attractiveness of salted food. The extant hypotheses are that most Na is infiltrated into our bodies via heavily salted industrialised food without our knowledge and that mere exposure early in life determines lifelong intake. However, these hypotheses are poorly evidenced and are meagre explanations for the comparable salt intake of people worldwide despite their markedly different diets. The love of salt begins at birth for some, vacillates in infancy, climaxes during adolescent growth, settles into separate patterns for men and women in adulthood and, with age, fades for some and persists for others. Salt adds flavour to food. It sustains and protects humans in exertion, may modulate their mood and contributes to their ailments. It may have as yet unknown benefits that may promote its delectability, and it generates controversy. An understanding of the predilection for salt should allow a more evidence-based and effective reduction of the health risks associated with Na surfeit and deficiency. The purpose of this brief review is to show the need for research into the determinants of salt intake by summarising the little we know.
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Metabolic adaptations during negative energy balance and their potential impact on appetite and food intake.
Casanova, N, Beaulieu, K, Finlayson, G, Hopkins, M
The Proceedings of the Nutrition Society. 2019;(3):279-289
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Abstract
This review examines the metabolic adaptations that occur in response to negative energy balance and their potential putative or functional impact on appetite and food intake. Sustained negative energy balance will result in weight loss, with body composition changes similar for different dietary interventions if total energy and protein intake are equated. During periods of underfeeding, compensatory metabolic and behavioural responses occur that attenuate the prescribed energy deficit. While losses of metabolically active tissue during energy deficit result in reduced energy expenditure, an additional down-regulation in expenditure has been noted that cannot be explained by changes in body tissue (e.g. adaptive thermogenesis). Sustained negative energy balance is also associated with an increase in orexigenic drive and changes in appetite-related peptides during weight loss that may act as cues for increased hunger and food intake. It has also been suggested that losses of fat-free mass (FFM) could also act as an orexigenic signal during weight loss, but more data are needed to support these findings and the signalling pathways linking FFM and energy intake remain unclear. Taken together, these metabolic and behavioural responses to weight loss point to a highly complex and dynamic energy balance system in which perturbations to individual components can cause co-ordinated and inter-related compensatory responses elsewhere. The strength of these compensatory responses is individually subtle, and early identification of this variability may help identify individuals that respond well or poorly to an intervention.
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Effect of physical exercise and training on gastrointestinal hormones in populations with different weight statuses.
Zouhal, H, Sellami, M, Saeidi, A, Slimani, M, Abbassi-Daloii, A, Khodamoradi, A, El Hage, R, Hackney, AC, Ben Abderrahman, A
Nutrition reviews. 2019;(7):455-477
Abstract
Several types of hormones exert control over appetite in humans. This narrative review explores the effects of exercise and training on the concentrations of gastrointestinal hormones in healthy and obese individuals. It focuses on the major hormones of appetite regulation: ghrelin, glucagon-like peptide 1, peptide YY, cholecystokinin, leptin, and oxyntomodulin. In normal-weight and overweight individuals, responses to most of these hormones depend on the intensity of exercise and training. However, findings in obese individuals are limited in number and, to some degree, contradictory. Although some gastrointestinal hormones have been studied extensively (eg, leptin), most have not been investigated systematically. Further research is required to confirm the effectiveness of exercise and training on gut hormones and to better understand the effect of gut hormones on appetite and hunger suppression in individuals with obesity. Investigations to elucidate the impact of various forms of exercise that have recently engaged the public interest, eg, high-intensity interval training or concurrent aerobic and resistance training, are warranted.
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Ghrelin forms in the modulation of energy balance and metabolism.
Gortan Cappellari, G, Barazzoni, R
Eating and weight disorders : EWD. 2019;(6):997-1013
Abstract
Ghrelin is a gastric hormone circulating in acylated (AG) and unacylated (UnAG) forms. This narrative review aims at presenting current emerging knowledge on the impact of ghrelin forms on energy balance and metabolism. AG represents ~ 10% of total plasma ghrelin, has an appetite-stimulating effect and is the only form for which a receptor has been identified. Moreover, other metabolic AG-induced effects have been reported, including the modulation of glucose homeostasis with stimulation of liver gluconeogenesis, the increase of fat mass and the improvement of skeletal muscle mitochondrial function. On the other hand, UnAG has no orexigenic effects, however recent reports have shown that it is directly involved in the modulation of skeletal muscle energy metabolism by improving a cluster of interlinked functions including mitochondrial redox activities, tissue inflammation and insulin signalling and action. These findings are in agreement with human studies which show that UnAG circulating levels are positively associated with insulin sensitivity both in metabolic syndrome patients and in a large cohort from the general population. Moreover, ghrelin acylation is regulated by a nutrient sensor mechanism, specifically set on fatty acids availability. These recent findings consistently point towards a novel independent role of UnAG as a regulator of muscle metabolic pathways maintaining energy status and tissue anabolism. While a specific receptor for UnAG still needs to be identified, recent evidence strongly supports the hypothesis that the modulation of ghrelin-related molecular pathways, including those involved in its acylation, may be a potential novel target in the treatment of metabolic derangements in disease states characterized by metabolic and nutritional complications.Level of evidence Level V, narrative review.
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Biological underpinnings from psychosocial stress towards appetite and obesity during youth: research implications towards metagenomics, epigenomics and metabolomics.
Michels, N
Nutrition research reviews. 2019;(2):282-293
Abstract
Psychosocial stress, uncontrolled eating and obesity are three interrelated epidemiological phenomena already present during youth. This broad narrative conceptual review summarises main biological underpinnings of the stress-diet-obesity pathway and how new techniques can further knowledge. Cortisol seems the main biological factor from stress towards central adiposity; and diet, physical activity and sleep are the main behavioural pathways. Within stress-diet, the concepts of comfort food and emotional eating are highlighted, as cortisol affects reward pathways and appetite brain centres with a role for insulin, leptin, neuropeptide Y (NPY), endocannabinoids, orexin and gastrointestinal hormones. More recently researched biological underpinnings are microbiota, epigenetic modifications and metabolites. First, the gut microbiota reaches the stress-regulating and appetite-regulating brain centres via the gut-brain axis. Second, epigenetic analyses are recommended as diet, obesity, stress and gut microbiota can change gene expression which then affects appetite, energy homeostasis and stress reactivity. Finally, metabolomics would be a good technique to disentangle stress-diet-obesity interactions as multiple biological pathways are involved. Saliva might be an ideal biological matrix as it allows metagenomic (oral microbiota), epigenomic and metabolomic analyses. In conclusion, stress and diet/obesity research should be combined in interdisciplinary collaborations with implementation of several -omics analyses.
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Sleep, Health, and Metabolism in Midlife Women and Menopause: Food for Thought.
Kravitz, HM, Kazlauskaite, R, Joffe, H
Obstetrics and gynecology clinics of North America. 2018;(4):679-694
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Abstract
Sleep and metabolism are essential components of health. Metabolic health depends largely on individual's lifestyle. Disturbances in sleep health, such as changes in sleep patterns that are associated with menopause/reproductive aging and chronologic aging, may have metabolic health consequences. Sleep restriction and age-related changes in sleep and circadian rhythms may influence changes in appetite and reproductive hormones, energy expenditure, and body adiposity. In this article, the authors describe how menopause-related sleep disturbance may affect eating behavior patterns, immunometabolism, immunometabolic dysfunction, and associations between sleep and metabolic outcomes.
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Fructooligosaccharides and appetite.
Korczak, R, Slavin, JL
Current opinion in clinical nutrition and metabolic care. 2018;(5):377-380
Abstract
PURPOSE OF REVIEW Dietary fiber may play a role in obesity prevention through reduction of body weight and control of appetite, however, not all fibers are created equally, and characteristics of fiber such as viscosity, fermentability and solubility may affect appetite differently. RECENT FINDINGS Although early studies supported that fructan fibers, including inulin, fructooligosaccharides, and oligofructose affected satiety, more recent studies are less supportive. We found that a higher dose of fiber such as oligofructose (16 g/day) is needed and for a longer duration (12-16 weeks) to detect differences in appetite and subsequent energy intake, whereas, practical amounts of fructooligosaccharides, less than 10 g/day, generally do not affect satiety or food intake. It should be noted that there are many sources of fructan fibers, both in native foods, chicory roots, agave, and Jerusalem artichokes and isolated forms that vary in chain length. SUMMARY Fructan fibers, which include fructooligosaccharides, oligofructose, and inulin, provided in low doses (<10 g/day), generally do not affect measures of human appetite including satiety or food intake and should not be recommended as a fiber with sole satiating power.