Altered gastric vagal mechanosensitivity in diet-induced obesity persists on return to normal chow and is accompanied by increased food intake

Jul 31, 2013International journal of obesity (2005)

Changes in stomach nerve sensitivity caused by high-fat diet continue after returning to normal food and are linked to eating more

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Abstract

After 24 weeks, both high-fat diet (HFD) and reverting to a standard diet (RFD) resulted in increased body weight and plasma leptin levels compared to the standard laboratory chow diet (SLD).

Gastric vagal afferents exhibit reduced sensitivity to mechanical stimuli in mice on a high-fat diet.
Leptin inhibits the response of gastric vagal afferents to tension in both HFD and RFD mice, but not in SLD mice.
Mucosal receptors in SLD and RFD mice respond positively to leptin, a response not observed in HFD mice.
Leptin receptor expression in the whole nodose remains unchanged, but is reduced in mucosal afferents of HFD and RFD mice.
The impairment of gastric vagal afferent function due to obesity is only partially reversible upon dietary change.

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BACKGROUND AND AIMS: Gastric vagal afferents convey satiety signals in response to mechanical stimuli. The sensitivity of these afferents is decreased in diet-induced obesity. Leptin, secreted from gastric epithelial cells, potentiates the response of vagal afferents to mechanical stimuli in lean mice, but has an inhibitory effect in high-fat diet (HFD)-induced obese mice. We sought to determine whether changes in vagal afferent function and response to leptin in obesity were reversible by returning obese mice consuming a HFD to standard laboratory chow diet (SLD).

METHODS: Eight-week-old female C57BL/6 mice were either fed a SLD (N=20) or HFD (N=20) for 24 weeks. A third group was fed a HFD for 12 weeks and then a SLD for a further 12 weeks (RFD, N=18). An in vitro gastro-oesophageal vagal afferent preparation was used to determine the mechanosensitivity of gastric vagal afferents and the modulatory effect of leptin (0.1-10 nM) was examined. Retrograde tracing and quantitative RT-PCR were used to determine the expression of leptin receptor (LepR) messenger RNA (mRNA) in whole nodose and specific cell bodies traced from the stomach.

RESULTS: After 24 weeks, both the HFD and RFD mice had increased body weight, gonadal fat mass, plasma leptin, plasma insulin and daily energy consumption compared with the SLD mice. The HFD and RFD mice had reduced tension receptor mechanosensitivity and leptin further inhibited responses to tension in HFD, RFD but not SLD mice. Mucosal receptors from both the SLD and RFD mice were potentiated by leptin, an effect not seen in HFD mice. LepR expression was unchanged in the whole nodose, but was reduced in the mucosal afferents of the HFD and RFD mice.

CONCLUSION: Disruption of gastric vagal afferent function by HFD-induced obesity is only partially reversible by dietary change, which provides a potential mechanism preventing maintenance of weight loss.

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Altered gastric vagal mechanosensitivity in diet-induced obesity persists on return to normal chow and is accompanied by increased food intake

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