The role of gut hormones and the hypothalamus in appetite regulation

Suzuki, Keisuke; Simpson, Katherine Anne; Minnion, James; Shillito, Joyceline C

doi:10.1507/endocrj.k10e-077

Cited by 256 publications

(184 citation statements)

References 169 publications

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“…neurons, which stimulate the food intake co-expressing neuropeptide Y (NPY) and agouti related peptide (AgRP), and neurons, which suppress the feeding co-expressing pro-opiomelanocortin (POMC) and cocaine-and amphetamine-regulated transcript (CART). Both types of the neurons project to the hypothalamic areas, which are involved in the control of appetite including the DMN, PVN, and LHA (Suzuki et al 2010) (Figure 2).…”

Section: Th E Hypothalamus Role In the Food Intake Controlmentioning

confidence: 99%

“…Th e orexigenic eff ect of NPY is mediated by stimulation of the hypothalamic Y1R and Y5R, in addition to the local inhibition of the POMC neurons in the ARC. In addition, AgRP acts as a selective antagonist at MC3R and MC4R in the PVN (Suzuki et al 2010).…”

Section: Th E Hypothalamus Role In the Food Intake Controlmentioning

confidence: 99%

“…Ob-Rb receptor belongs to the type I cytokine receptor family and exists in fi ve distinct isoforms (splice variants) named as Ob-Ra, Ob-Rb, Ob-Rc, Ob-Rd, and Ob-Re. Only the Ob-Rb isoform contains a long intracellular domain essential for the biological actions of leptin (Suzuki et al 2010).…”

Section: Role Of Peripheral Adiposity Signalsmentioning

confidence: 99%

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Central and peripheral control of food intake

Abdalla

2017

Endocrine Regulations

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Th e maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive. Th e body weight depends on the balance between the energy intake and energy expenditure. Increased food intake over the energy expenditure of prolonged time period results in an obesity. Th e obesity has become an important worldwide health problem, even at low levels. Th e obesity has an evil eff ect on the health and is associated with a shorter life expectancy. A complex of central and peripheral physiological signals is involved in the control of the food intake. Centrally, the food intake is controlled by the hypothalamus, the brainstem, and endocannabinoids and peripherally by the satiety and adiposity signals. Comprehension of the signals that control food intake and energy balance may open a new therapeutic approaches directed against the obesity and its associated complications, as is the insulin resistance and others. In conclusion, the present review summarizes the current knowledge about the complex system of the peripheral and central regulatory mechanisms of food intake and their potential therapeutic implications in the treatment of obesity. Th e maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive (Jequier and Tappy 1999). As a compensatory mechanism, hunger increases and energy expenditure decreases the weight loss. However, opposite responses are triggered when body weight increases. Body weight can change only when energy intake is not equal to energy expenditure over a given period of time (Bray et al. 2012). A complex physiological control system is involved in the maintenance of the energy balance. Th is system includes aff erent signals from the periphery about the state of the energy stores and eff erent signals that affect the energy intake and expenditure (Sandoval et al. 2008). Th is regulatory system is formed by multiple interactions between the gastrointestinal tract (GIT), adipose tissue, and the central nervous system (CNS). It is infl uenced by behavioral, sensorial, autonomic, nutritional, and endocrine mechanisms (Boguszewski et al. 2010). Satiety and adiposity signalsTh e food intake control includes a short-term regulation, which determines the beginning and the end of a meal (hunger and satiation) and the interval between the meals (satiety) and a long-term regulation with factors (signals of adiposity), which help to regulate the body energy depots (Cummings and Overduin 2007).Th e satiation means a suppression of the hunger and termination of the food intake aft er ingestion of Unauthenticated Download Date | 5/11/18 9:54 AM

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Section: Th E Hypothalamus Role In the Food Intake Controlmentioning

confidence: 99%

Section: Th E Hypothalamus Role In the Food Intake Controlmentioning

confidence: 99%

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Central and peripheral control of food intake

Abdalla

2017

Endocrine Regulations

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“…Several mechanisms could have been responsible for these differences. Enhanced satiety and reduced hunger immediately after HENSD supplementation can be attributed to significantly higher plasma concentrations of PYY and CCK, which are known to elicit anorexigenic effects (Chaudhri, Field, & Bloom, 2008;Suzuki, Simpson, Minnion, Shillito, & Bloom, 2010) and to insulin, which plays a role in appetite regulation of lean individuals (A. Flint et al, 2007).…”

Section: Hensd Placebomentioning

confidence: 99%

Response of appetite and potential appetite regulators following intake of high energy nutritional supplements

et al. 2015

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Keywords:High energy supplements Appetite Appetite hormones Gastric emptying Thermogenesis Control of food intake a b s t r a c t Background:The net clinical benefit of high-energy nutritional supplements (HENSDs) consumption is lower than expected. Objectives: To investigate the extent to which consumption of oral HENSD in the fasted state reduces energy intake in slim females during consecutive breakfast and lunch, and whether this relates to changes in appetite and metabolic appetite regulators. Design: Twenty three females of 24.4 ± 2.8 years with BMI of 18.2 ± 0.8 kg/m 2 consumed HENSD (2.5 MJ) or PLACEBO (0.4 MJ) in fasted state in a single blind randomized cross-over study. Appetite and metabolic rate measurements and blood collection were conducted prior to and during 240 min after the intake of the supplements. Energy intake was recorded during ad libitum buffet breakfast and lunch served 60 min and 240 min post supplementation respectively. Results: Energy intake during breakfast was significantly (P < 0.01) lower in the HENSD trial but the net cumulative effect on energy intake was 1.07 ± 0.34 MJ higher in the HENSD compared to PLACEBO. Plasma concentration of CCK and PYY and insulin and were significantly (P < 0.05) higher in the HENSD trial while appetite measures were not significantly different between HENSD and PLACEBO trials. Correlations for the within participant relations between the responses of plasma hormones and appetite scores were significant (P < 0.05) for PYY and insulin but not CCK. The energy expended above resting metabolic rate was significantly (P < 0.05) higher in the HENDS trial but relative increase in energy expenditure was not significantly different between the two trials. Conclusion: Oral high-energy nutritional supplements have a partial and relatively short lived suppressive action on energy intake and can be expected to increase net energy intake by approximately half the energy value of the supplement consumed.

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“…Given the fact that diabetes develops when the insulin secretion by beta cells is insufficient to compensate for insulin resistance [22,23] and GLP-1 reportedly inhibits apoptosis in humans, the increase in the GLP-1 concentration may be important for improving beta cell function [24]. In addition, the increase in GLP-1 may protect against obesity because of the anti-obesity effect GLP-1 [25][26][27][28].…”

Section: A B a Bmentioning

confidence: 99%