title: Maintenance on a ketogenic diet: voluntary exercise, adiposity and neuroendocrine effects.
abstract: BACKGROUND
  Adherence to low-carbohydrate, ketogenic diets (KDs) has been associated with greater weight loss in the short-term than low-fat, calorie-restricted diets. However, consumption of KDs may result in decreased voluntary exercise and thus render long-term weight loss and maintenance of weight loss difficult.
  
  
  METHODS
  Rats were maintained on either a non-ketogenic chow (CH) diet or a low-carbohydrate, KD for 6 weeks. Half of each dietary group was sedentary, whereas the other half was given access to a running wheel. Running wheel activity (total distance and meters per minute), plasma leptin and insulin, adiposity, and hypothalamic mRNA for neuropeptide Y and proopiomelanocortin (POMC) were measured to assess activity-related effects in animals maintained on KD.
  
  
  RESULTS
  With access to a running wheel, rats on KD engaged in similar levels of voluntary activity as CH rats and both dietary groups decreased caloric intake. Caloric intake increased over time such that it was significantly greater than sedentary controls after 1 month of access to the wheels, however body weight remained decreased. Sedentary rats maintained on KD had increased adiposity and plasma leptin levels and decreased hypothalamic POMC mRNA, as compared to sedentary CH rats. KD rats with access to a running wheel had similar levels of adiposity and plasma leptin levels as CH rats with access to running wheels, but significantly increased POMC mRNA in the arcuate.
  
  
  CONCLUSIONS
  We demonstrate that maintenance on KD does not inhibit voluntary activity in a running wheel. Furthermore, prevention of KD-related increased adiposity and plasma leptin, as measured in sedentary KD rats, significantly increases levels of the anorexigenic neuropeptide POMC mRNA.
authors.affiliation: Department of Psychological Sciences, Ingestive Behavior Research Center, Purdue University, 703 Third Street, West Lafayette, IN 47907, USA. kkinzig@purdue.edu
authors.forename: K P
authors.initials: KP
authors.lastname: Kinzig
authors.forename: R J
authors.initials: RJ
authors.lastname: Taylor
mesh_terms: D050154:Adiposity / Q000502:physiology*; D000818:Animals; D001835:Body Weight / Q000502:physiology*; D050528:Diet, Carbohydrate-Restricted; D055423:Diet, Ketogenic; D007031:Hypothalamus / Q000378:metabolism / Q000502:physiology*; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood*; D008297:Male; D009043:Motor Activity / Q000502:physiology*; D009478:Neuropeptide Y / Q000097:blood / Q000235:genetics; D010805:Physical Conditioning, Animal; D011333:Pro-Opiomelanocortin / Q000097:blood / Q000235:genetics; D012333:RNA, Messenger / Q000097:blood; D051381:Rats; D020318:Rats, Long-Evans; D015398:Signal Transduction / Q000502:physiology
chemical_list: D007328:Insulin; D020738:Leptin; D009478:Neuropeptide Y; D012333:RNA, Messenger; D011333:Pro-Opiomelanocortin