Neuroendocrine regulation of food intake

Chaptini, Louis; Peikin, Steven R.

doi:10.1097/mog.0b013e3282f3f4d8

Cited by 18 publications

(7 citation statements)

References 60 publications

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“…Ghrelin, which is secreted into the circulation from intestinal structures such as the stomach, is the most recently-discovered anabolic hormone regulating energy consumption and storage in the brain and peripheral tissues through such effects as growth, increased appetite, fat accumulation and increased gluconeogenesis (1,8). weight gain (1).…”

Section: Discussionmentioning

confidence: 99%

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Effect of orlistat on the total ghrelin and leptin levels in obese patients

et al. 2009

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Obesity, characterized by hyperleptinemia and hypoghrelinemia, has become a major health problem all over the world and is associated with an increased risk of complications including insulin resistance, hypertension, dyslipidemia, diabetes mellitus and atherosclerosis. The use of the pancreatic lipase inhibitor Orlistat can help seriously overweight people to achieve and maintain weight loss. The aim of our study was to compare the serum leptin and ghrelin levels in obese subjects who take orlistat with those receiving only dietary treatment. Twenty-one obese patients and 10 control subjects participated. The obese patients were divided into two groups; one group (n=11) took orlistat (120 mg, 3 times daily) and received dietary treatment and the other (n=10) only received the dietary treatment. The study lasted twelve weeks. The concentrations of serum ghrelin, leptin, insulin and C-peptide, and routine biochemical parameters, were measured in both groups. The serum ghrelin level was higher in control (183+/-62 fmol/ml) than obese (59+/-30 fmol/ml) subjects while the plasma leptin level was lower in control (8.7+/-12 microg/L) than obese (36.7+/-19 microg/L) subjects (all p<0.001). BMI and the total blood cholesterol, LDL and triglyceride levels fell significantly after both orlistat and dietary treatment in the obese subjects (all p<0.01), and the plasma ghrelin level rose (p<0.01). The leptin level demonstrated the opposite trend in both groups but only the patients taking orlistat showed a significant change (p<0.05).Taken together, these results show that orlistat has no effect on body weight in obese subjects additional to that conferred by a non-pharmacological life-style intervention. We therefore conclude that weight lost rather than type of treatment might be more valuable in obesity.

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Section: Discussionmentioning

confidence: 99%

“…Diet and physical activity affect leptin levels, which are also associated with negative energy balance (8). Leptin inhibits lipogenesis and activates lipolysis (3).…”

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confidence: 99%

Effect of orlistat on the total ghrelin and leptin levels in obese patients

et al. 2009

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“…leptin, insulin, ghrelin) that act in concert with several pathways in the brain (e.g. NPY, AgRP) to promote feeding behaviour (for reviews, see Chaptini and Peikin, 2008;Speakman and Król, 2005a). Endocrine systems cannot, however, be stimulated indefinitely because receptors become saturated.…”

Section: Discussionmentioning

confidence: 99%

Limits to sustained energy intake. XIV. Heritability of reproductive performance in mice

Vaanholt

Sinclair

Speakman

2013

Journal of Experimental Biology

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SUMMARYLimits to sustained energy intake (SusEI) are important because they constrain many aspects of animal performance. Individual variability in SusEI may be imposed by genetic factors that are inherited from parents to offspring. Here, we investigated heritability of reproductive performance in MF1 mice. Food intake, milk energy output (MEO) and litter mass were measured in mothers (F 0 ) and daughters (F 1 ) that were raising litters of 10 pups. Cross-fostering was designed so that half of each litter consisted of biological offspring and the rest came from one unrelated female (i.e. fostered pups). Food intake increased linearly during early lactation and reached a plateau during late lactation (day 9-13, called the asymptotic food intake, FI AS , equivalent to SusEI). Parent-offspring regression showed that FI AS , MEO and litter mass were all positively and significantly related between mothers and their biological daughters, but no significant relationships were found between the same traits for mothers and fostered daughters. FI AS at peak lactation was significantly correlated to adult food intake and body mass when the mice were 6months old and not lactating. In conclusion, a large part of the variation in FI AS could be explained by genetic variation or maternal effects in pregnancy whereas non-genetic maternal effects in lactation were negligible. As a consequence, biological daughters of mothers with high reproductive performance (i.e. high milk production and hence higher litter mass at weaning) had a better reproductive performance themselves, independent of the mother that raised them during lactation.

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“…6,7 The hypothalamus is involved in 2 major pathways that mediate appetite and eating behavior (figure 1): an appetite-stimulating pathway, with key peptides including ghrelin and agouti-related peptide (AgRP), and an appetitesuppressing pathway, with key peptides including leptin. 8 Oxytocin, which is produced in the hypothalamus, is an important component of the pathways activated by leptin, and is believed to decrease food intake. 9 Other peptides released peripherally include peptide tyrosine tyrosine (PYY) and cholecystokinin (CCK), and participate by inhibiting food intake.…”

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confidence: 99%

Eating behavior in frontotemporal dementia

et al. 2015

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Objective: To contrast the relationships of hormonal eating peptides and hypothalamic volumes to eating behavior and metabolic changes (body mass index [BMI]) in behavioral variant frontotemporal dementia (bvFTD) and semantic variant primary progressive aphasia (svPPA).Methods: Seventy-five patients with dementia (19 bvFTD, 26 svPPA, and 30 Alzheimer disease dementia) and 23 controls underwent fasting blood analyses of leptin, ghrelin, cholecystokinin, peptide tyrosine tyrosine (PYY), and agouti-related peptide (AgRP) levels. On brain MRI anterior, posterior, and total hypothalamic volumes were measured. Relationships between endocrine measures, hypothalamic volumes, eating behaviors, and BMI were investigated.Results: Levels of AgRP were higher in patients with bvFTD (69 6 89 pg/mL) and svPPA (62 6 81 pg/mL) compared with controls (23 6 19 pg/mL, p , 0.01). No differences were found for leptin, oxytocin, cholecystokinin, ghrelin, and PYY levels. Patients with bvFTD and svPPA had higher scores on questionnaires measuring eating behaviors. Atrophy of the posterior and total hypothalamus was observed in the bvFTD group only. Linear regression modeling revealed that leptin and AgRP levels predicted BMI. Conclusion:Eating abnormalities are multifactorial in FTD. In bvFTD, they are in part related to hypothalamic degeneration, with potential disintegration of the network connections between the hypothalamus and orbitofrontal cortex/reward pathways. In svPPA, although hypothalamic volumes are preserved, this group experiences elevated AgRP levels similar to bvFTD, which predicts BMI in both groups. This finding highlights the potential key role of AgRP in eating and metabolic changes and provides a potential target for treatment to modify disease progression. Alterations in eating behavior are one of the diagnostic criteria for behavioral variant frontotemporal dementia (bvFTD).

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Neuroendocrine regulation of food intake

Abstract: Complex and intricate neuroendocrine pathways control food intake and energy homeostasis. The increasing understanding of the different components orchestrating the regulation of food intake provides new and exciting targets for much needed pharmacotherapy for obesity.

Cited by 18 publications

References 60 publications

Effect of orlistat on the total ghrelin and leptin levels in obese patients

Effect of orlistat on the total ghrelin and leptin levels in obese patients

Limits to sustained energy intake. XIV. Heritability of reproductive performance in mice

Eating behavior in frontotemporal dementia

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