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Nutrition. 2016 Jun;32(6):709-15. doi: 10.1016/j.nut.2015.12.034. Epub 2015 Dec 30.

High-fat diet increases ghrelin-expressing cells in stomach, contributing to obesity.

Author information

1
Inserm UMR1073, Nutrition, Gut and Brain Laboratory, Rouen, France; Institute for Research and Innovation in Biomedicine (IRIB), Rouen University, Normandy University, Rouen, France.
2
Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
3
Inserm UMR1073, Nutrition, Gut and Brain Laboratory, Rouen, France; Institute for Research and Innovation in Biomedicine (IRIB), Rouen University, Normandy University, Rouen, France; Rouen University Hospital, CHU Charles Nicolle, Rouen, France.
4
Inserm UMR1073, Nutrition, Gut and Brain Laboratory, Rouen, France; Institute for Research and Innovation in Biomedicine (IRIB), Rouen University, Normandy University, Rouen, France. Electronic address: Serguei.Fetissov@univ-rouen.fr.

Abstract

OBJECTIVES:

Mechanisms of high-fat diet (HFD)-induced obesity may involve ghrelin, an orexigenic and adipogenic hormone secreted by the stomach. Previous studies showed that obese subjects may display higher numbers of ghrelin-producing cells and increased affinity of plasma immunoglobulins (Ig) for ghrelin, protecting it from degradation. The aim of this study was to determine if a HFD in mice would increase the number of ghrelin-expressing cells and affinity of ghrelin-reactive IgG.

METHODS:

Obesity in mice was induced by consumption of a 13-wk HFD. The number of preproghrelin mRNA-expressing cells in the stomach was analyzed by in situ hybridization and compared with chow-fed, nonobese controls and with genetically obese ob/ob mice. Affinity of ghrelin-reactive IgG was analyzed using surface plasmon resonance. Plasma levels of ghrelin and des-acyl ghrelin were measured.

RESULTS:

HFD resulted in 30% of body fat content versus only 8% in controls (P < 0.001). The number of preproghrelin mRNA-producing cells was 15% (P < 0.05) higher in HFD-fed mice than in controls, contrasting with ob/ob mice, having a 41% (P < 0.001) decrease. Both models of obesity had normal plasma levels of ghrelin but a decrease of its des-acylated form. Ghrelin-reactive IgG affinity was found in the micromolar range with mean values of the dissociation equilibrium constant 1.5-fold (P < 0.05) lower in HFD-fed versus control mice.

CONCLUSION:

Results from the present study showed that HFD in mice induces obesogenic changes, including increased numbers of ghrelin precursor-expressing cells and increased affinity of ghrelin-reactive IgG. Such changes may contribute to the mechanisms of HFD-induced obesity.

KEYWORDS:

Autoantibodies; Ghrelin; High-fat diet; In situ hybridization; Obesity

PMID:
26856650
DOI:
10.1016/j.nut.2015.12.034
[Indexed for MEDLINE]

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