The hepatic vagus mediates fat-induced inhibition of diabetic hyperphagia

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Diabetic rats both overeat high-carbohydrate diet and have altered hypothalamic neuropeptide Y (NPY) and corticotropin-releasing factor (CRF). In contrast, a high-fat diet reduces caloric intake of diabetics to nor- mal, reflected by normal hypothalamic NPY and CRF content. How the brain senses these changes in diet is unknown. To date, no hormonal changes explain these diet-induced changes in caloric intake. We tested whether the common branch of the hepatic vagus medi- ates the fat signal. We presented fat in two ways. First, diabetic and vehicle-treated rats were offered a cup of lard in addition to their normal high-carbohydrate diet. Second, we switched diabetic rats from high-carbohy- drate diet to high-fat diet, without choice. In streptozo- tocin-treated rats, both methods resulted in fat-induced inhibition of caloric intake and normalization of hypo- thalamic neuropeptides to nondiabetic levels. Strik- ingly, common branch hepatic vagotomy (unlike gastro- duodenal vagotomy) entirely blocked these fat-induced changes. Although a shift in hepatic energy status did not explain the lard-induced changes in diabetic rats, the data suggested that common hepatic branch vagot- omy does not interfere with hepatic energy status. Furthermore, common branch hepatic vagotomy with- out diabetes induced indexes of obesity. Abnormal func- tion of the hepatic vagus, as occurs in diabetic neuro- pathy, may contribute to diabetic obesity.




La Fleur, S. E., Ji, H., Manalo, S. L., Friedman, M. I., & Dallman, M. F. (2003). The hepatic vagus mediates fat-induced inhibition of diabetic hyperphagia. Diabetes, 52(9), 2321–2330.

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