Frank A Duca1, Shahbaz Katebzadeh2, Mihai Covasa3,4. 1. Toronto General Research Institute and Department of Medicine, University Health Network, Toronto, Ontario, Canada. 2. College of Dental Medicine, Western University of the Health Sciences, Pomona, California, USA. 3. College of Osteopathic Medicine, Department of Basic Medical Sciences, Western University of the Health Sciences, Pomona, California, USA. 4. Department of Health and Human Development, University "Stefan Cel Mare" Suceava, Suceava, Romania.
Abstract
OBJECTIVE: Increased consumption of a high-fat (HF) diet is a salient contributor to obesity; however, how diminished satiation signaling contributes to overconsumption and obesity development remains poorly understood. METHODS: Using obese-prone (OP) and obese-resistant (OR) rats, we tested feeding responses to intragastric liquid meal replacement, prior and after HF feeding. Next, chow- and HF-fed OP and OR rats were tested for sensitivity to intraduodenal glucose, intralipid, and meal replacement loads. To examine the role of glucagon-like peptide-1 (GLP-1) and vagal signaling, animals were treated with exendin-9, GLP-1 receptor antagonist, prior to meal replacement infusion, and Fos-like immunoreactivity (Fos-Li) in the dorsal hindbrain was examined after infusion. RESULTS: OP and OR rats reduced chow intake equally following gastric liquid meal; however, after 2 weeks of HF feeding, intragastric meal replacement reduced food intake less in OP than OR. Similarly, HF feeding, but not chow, diminished the suppressive effects of intraduodenal meal replacement, glucose, and intralipid in OP compared to OR. This effect was associated with lower Fos-Li expression in the dorsal hindbrain of OP rats. Finally, exendin-9 failed to attenuate reduction of food intake by meal replacement in OP rats during HF feeding. CONCLUSIONS: Susceptibility to obesity coupled with HF feeding results in rapid impairments in nutrient-induced satiation through blunted responses in endogenous GLP-1 and hindbrain vagal afferent signaling.
OBJECTIVE: Increased consumption of a high-fat (HF) diet is a salient contributor to obesity; however, how diminished satiation signaling contributes to overconsumption and obesity development remains poorly understood. METHODS: Using obese-prone (OP) and obese-resistant (OR) rats, we tested feeding responses to intragastric liquid meal replacement, prior and after HF feeding. Next, chow- and HF-fed OP and OR rats were tested for sensitivity to intraduodenal glucose, intralipid, and meal replacement loads. To examine the role of glucagon-like peptide-1 (GLP-1) and vagal signaling, animals were treated with exendin-9, GLP-1 receptor antagonist, prior to meal replacement infusion, and Fos-like immunoreactivity (Fos-Li) in the dorsal hindbrain was examined after infusion. RESULTS: OP and OR rats reduced chow intake equally following gastric liquid meal; however, after 2 weeks of HF feeding, intragastric meal replacement reduced food intake less in OP than OR. Similarly, HF feeding, but not chow, diminished the suppressive effects of intraduodenal meal replacement, glucose, and intralipid in OP compared to OR. This effect was associated with lower Fos-Li expression in the dorsal hindbrain of OP rats. Finally, exendin-9 failed to attenuate reduction of food intake by meal replacement in OP rats during HF feeding. CONCLUSIONS: Susceptibility to obesity coupled with HF feeding results in rapid impairments in nutrient-induced satiation through blunted responses in endogenous GLP-1 and hindbrain vagal afferent signaling.
Authors: Jesse L Carlin; Sarah E McKee; Tiffany Hill-Smith; Nicola M Grissom; Robert George; Irwin Lucki; Teresa M Reyes Journal: Neuroscience Date: 2016-04-08 Impact factor: 3.590
Authors: Calyn B Maske; Isabel I Coiduras; Zeleen E Ondriezek; Sarah J Terrill; Diana L Williams Journal: Obesity (Silver Spring) Date: 2020-04-01 Impact factor: 5.002