title: Hepatic branch vagotomy, like insulin replacement, promotes voluntary lard intake in streptozotocin-diabetic rats.
abstract: Although high insulin concentrations reduce food intake, low insulin concentrations promote lard intake over chow, possibly via an insulin-derived, liver-mediated signal. To investigate the role of the hepatic vagus in voluntary lard intake, streptozotocin-diabetic rats with insulin or vehicle replaced into either the superior mesenteric or jugular veins received a hepatic branch vagotomy (HV) or a sham operation. All rats received a pellet of corticosterone that clamped the circulating steroid at moderately high concentrations to enhance lard intake. After 5 d of recovery, rats were offered the choice of lard and chow for 5 d. In streptozotocin-diabetic rats, HV, like insulin replacement, restored lard intake to nondiabetic levels. Consequently, this reduced chow intake without affecting total caloric intake, and insulin site-specifically increased white adipose tissue weight. HV also ablated the effects of insulin on reducing circulating glucose levels and attenuated the streptozotocin-induced weight loss in most groups. Collectively, these data suggest that the hepatic vagus normally inhibits lard intake and can influence glucose homeostasis and the pattern of white adipose tissue deposition. These actions may be modulated by insulin acting both centrally and peripherally.
authors.affiliation: Department of Physiology, Box 0444, University of California, San Francisco, 513 Parnassus Avenue, San Francisco, California 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 / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D003345:Corticosterone / Q000008:administration & dosage / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000503:physiopathology / Q000628:therapy*; D004041:Dietary Fats / Q000008:administration & dosage / Q000378:metabolism*; D002149:Energy Intake / Q000187:drug effects; D005230:Fatty Acids, Nonesterified / Q000097:blood; D006003:Glycogen / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007328:Insulin / Q000097:blood / Q000494:pharmacology*; D007657:Ketone Bodies / Q000097:blood; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013311:Streptozocin; D013997:Time Factors; D014280:Triglycerides / Q000097:blood; D014628:Vagotomy / Q000379:methods*; D014630:Vagus Nerve / Q000503:physiopathology
chemical_list: D001786:Blood Glucose; D004041:Dietary Fats; D005230:Fatty Acids, Nonesterified; D007004:Hypoglycemic Agents; D007328:Insulin; D007657:Ketone Bodies; D014280:Triglycerides; D013311:Streptozocin; D006003:Glycogen; C029310:lard; D003345:Corticosterone