title: Cerebral blood flow and glucose metabolism in appetite-related brain regions in type 1 diabetic patients after treatment with insulin detemir and NPH insulin: a randomized controlled crossover trial.
abstract: OBJECTIVE
  To test the hypothesis that insulin detemir, which is associated with less weight gain than other basal insulin formulations, exerts its weight-modulating effects by acting on brain regions involved in appetite regulation, as represented by altered cerebral blood flow (CBF) or cerebral glucose metabolism (CMRglu).
  
  
  METHODS
  Twenty-eight male type 1 diabetic patients (age 36.9 ± 9.7 years, BMI 24.9 ± 2.7 kg/m(2), A1C 7.5 ± 0.6%) successfully completed a randomized crossover study, consisting of two periods of 12-week treatment with either insulin detemir or NPH insulin, both in combination with prandial insulin aspart. After each treatment period, patients underwent positron emission tomography scans to measure regional CBF and CMRglu.
  
  
  RESULTS
  After 12 weeks, A1C, daily insulin doses, fasting insulin, and blood glucose levels were similar between treatments. Insulin detemir resulted in body weight loss, whereas NPH insulin induced weight gain (between-treatment difference 1.3 kg; P = 0.02). After treatment with insulin detemir relative to NPH insulin, CBF was higher in brain regions involved in appetite regulation, whereas no significant difference in CMRglu was observed.
  
  
  CONCLUSIONS
  Treatment with insulin detemir versus NPH insulin resulted in weight loss, paralleled by increased CBF in appetite-related brain regions in the resting state, in men with well-controlled type 1 diabetes. These findings lend support to the hypothesis that a differential effect on the brain may contribute to the consistently observed weight-sparing effect of insulin detemir.
authors.affiliation: Corresponding author: Larissa W. van Golen, l.vangolen@vumc.nl.
authors.forename: Larissa W
authors.initials: LW
authors.lastname: van Golen
authors.forename: Richard G
authors.initials: RG
authors.lastname: Ĳzerman
authors.forename: Marc C
authors.initials: MC
authors.lastname: Huisman
authors.forename: Jolanda F
authors.initials: JF
authors.lastname: Hensbergen
authors.forename: Roel P
authors.initials: RP
authors.lastname: Hoogma
authors.forename: Madeleine L
authors.initials: ML
authors.lastname: Drent
authors.forename: Adriaan A
authors.initials: AA
authors.lastname: Lammertsma
authors.forename: Michaela
authors.initials: M
authors.lastname: Diamant
mesh_terms: D000293:Adolescent; D000328:Adult; D001066:Appetite / Q000502:physiology; D001921:Brain / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000502:physiology*; D018592:Cross-Over Studies; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D005260:Female; D005500:Follow-Up Studies; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007004:Hypoglycemic Agents / Q000008:administration & dosage; D021621:Imaging, Three-Dimensional; D000069057:Insulin Detemir; D007336:Insulin, Isophane / Q000008:administration & dosage*; D049528:Insulin, Long-Acting / Q000008:administration & dosage*; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D012039:Regional Blood Flow / Q000502:physiology*; D012189:Retrospective Studies; D055815:Young Adult
chemical_list: D007004:Hypoglycemic Agents; D049528:Insulin, Long-Acting; D000069057:Insulin Detemir; D007336:Insulin, Isophane; D005947:Glucose