title: Increased prevalence of impaired fasting glucose in MEN1 gene mutation carriers.
abstract: OBJECTIVE
  Multiple endocrine neoplasia type 1 (MEN1) is a hereditary syndrome characterized by parathyroid, gastroenteropancreatic, pituitary and adrenal tumours. Cardiovascular disease has been identified as an important cause of death in MEN1 patients. Menin, the product of the MEN1 gene, is a co-activator for peroxisome proliferator-activated receptor-γ and the vitamin D receptor, which are involved in glucose metabolism. We aimed to compare insulin sensitivity and prevalence of impaired fasting glucose and diabetes mellitus between MEN1 patients and controls.
  
  
  METHODS
  Cross-sectional study.
  
  
  METHODS
  Sixty-three MEN1 gene mutation carriers (44% men, mean age 41 years) from 22 kindreds and 126 unrelated controls matched for gender, age and BMI.
  
  
  METHODS
  Fasting glucose levels were categorized and compared using WHO criteria. Homeostasis model assessment (HOMA) was used as a measure of insulin resistance.
  
  
  RESULTS
  Homeostasis model assessment was significantly increased in MEN1 patients compared with controls (3·0 ± 2·0 vs 2·0 ± 1·0, P < 0·05). In MEN1 patients, HOMA was associated with BMI, but not with age, calcium and gastrin levels. Using logistic regression analysis, the presence of hyperparathyroidism, pancreatic lesions and various other manifestations was not associated with HOMA. Impaired fasting glucose was more prevalent in MEN1 compared with controls (17%vs 6%, P < 0·05). Three MEN1 patients (5%) compared with four controls (3%) were diabetic (not significant).
  
  
  CONCLUSIONS
  Multiple endocrine neoplasia type 1 patients had decreased insulin sensitivity and higher prevalence of impaired fasting glucose compared with controls, which was unrelated to MEN1 manifestations. Impaired glucose metabolism may result in increased risk of cardiovascular disease in MEN1 patients.
authors: Department of Internal Medicine and Endocrinology, University Medical Center, Utrecht, The Netherlands.
authors: J P H
authors: JP
authors: van Wijk
authors: K M A
authors: KM
authors: Dreijerink
authors: C R C
authors: CR
authors: Pieterman
authors: C J M
authors: CJ
authors: Lips
authors: P M J
authors: PM
authors: Zelissen
authors: G D
authors: GD
authors: Valk
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000235:genetics* / Q000378:metabolism*; D005260:Female; D020022:Genetic Predisposition to Disease; D006706:Homeostasis; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics; D008297:Male; D009154:Mutation; D011518:Proto-Oncogene Proteins / Q000235:genetics* / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; C105373:MEN1 protein, human; D011518:Proto-Oncogene Proteins