title: Afferent signalling through the common hepatic branch of the vagus inhibits voluntary lard intake and modifies plasma metabolite levels in rats.
abstract: The common hepatic branch of the vagus nerve is a two-way highway of communication between the brain and the liver, duodenum, stomach and pancreas that regulates many aspects of food intake and metabolism. In this study, we utilized the afferent-specific neurotoxin capsaicin to examine if common hepatic vagal sensory afferents regulate lard intake. Rats implanted with a corticosterone pellet were made diabetic using streptozotocin (STZ) and a subset received steady-state exogenous insulin replacement into the superior mesenteric vein. These were compared with non-diabetic counterparts. Each group was then subdivided into those whose common hepatic branch of the vagus was treated with vehicle or capsaicin. Five days after surgery, the rats were offered the choice of chow and lard to consume for a further 5 days. The STZ-diabetic rats ate significantly less lard than the non-diabetic rats. Capsaicin treatment restored lard intake to that of the insulin-replaced, STZ-diabetic rats, but modified neither chow nor total caloric intake. This increased lard intake led to selective fat deposition into the mesenteric white adipose tissue depot, as opposed to an increase in all visceral fat pad depots evident after insulin replacement-induced lard intake. Capsaicin treatment also increased the levels of circulating glucose and triglycerides and negated the actions of insulin on these and free fatty acids and ketone bodies. Collectively, these data suggest that afferent signalling through the common hepatic branch of the vagus inhibits lard, but not chow, intake, directs fat deposition and regulates plasma metabolite levels.
authors.affiliation: Department of Physiology, University of California San Francisco, San Francisco, CA 94143, USA. james.warne@ucsf.edu
authors.forename: James P
authors.initials: JP
authors.lastname: Warne
authors.forename: Michelle T
authors.initials: MT
authors.lastname: Foster
authors.forename: Hart F
authors.initials: HF
authors.lastname: Horneman
authors.forename: Norman C
authors.initials: NC
authors.lastname: Pecoraro
authors.forename: Abigail B
authors.initials: AB
authors.lastname: Ginsberg
authors.forename: Susan F
authors.initials: SF
authors.lastname: Akana
authors.forename: Mary F
authors.initials: MF
authors.lastname: Dallman
mesh_terms: D052436:Adipose Tissue, White / Q000473:pathology; D000311:Adrenal Glands / Q000473:pathology; D000344:Afferent Pathways / Q000503:physiopathology; D000818:Animals; D015415:Biomarkers / Q000097:blood*; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D002211:Capsaicin / Q000494:pharmacology; D003345:Corticosterone / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D004041:Dietary Fats / Q000008:administration & dosage / Q000378:metabolism*; D005247:Feeding Behavior / Q000187:drug effects; D005518:Food Preferences; D005934:Glucagon / Q000097:blood; D006003:Glycogen / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000494:pharmacology / Q000627:therapeutic use; D007328:Insulin / Q000097:blood / Q000494:pharmacology / Q000627:therapeutic use; D020738:Leptin / Q000097:blood; D008055:Lipids / Q000097:blood; D008099:Liver / Q000294:innervation* / Q000378:metabolism; D008297:Male; D009929:Organ Size; D051381:Rats; D017207:Rats, Sprague-Dawley; D013154:Spleen / Q000473:pathology; D013950:Thymus Gland / Q000473:pathology; D013997:Time Factors; D014630:Vagus Nerve / Q000187:drug effects / Q000503:physiopathology*
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D004041:Dietary Fats; D007004:Hypoglycemic Agents; D007328:Insulin; D020738:Leptin; D008055:Lipids; D006003:Glycogen; D005934:Glucagon; D002211:Capsaicin; C029310:lard; D003345:Corticosterone