PMID- 21726266
OWN - NLM
STAT- MEDLINE
DCOM- 20120813
LR  - 20111207
IS  - 1365-2265 (Electronic)
IS  - 0300-0664 (Linking)
VI  - 76
IP  - 1
DP  - 2012 Jan
TI  - Increased prevalence of impaired fasting glucose in MEN1 gene mutation carriers.
PG  - 67-71
LID - 10.1111/j.1365-2265.2011.04166.x [doi]
AB  - 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-gamma 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. DESIGN: Cross-sectional study. PATIENTS: 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. MEASUREMENTS: 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.
CI  - (c) 2011 Blackwell Publishing Ltd.
FAU - van Wijk, J P H
AU  - van Wijk JP
AD  - Department of Internal Medicine and Endocrinology, University Medical Center, 
      Utrecht, The Netherlands.
FAU - Dreijerink, K M A
AU  - Dreijerink KM
FAU - Pieterman, C R C
AU  - Pieterman CR
FAU - Lips, C J M
AU  - Lips CJ
FAU - Zelissen, P M J
AU  - Zelissen PM
FAU - Valk, G D
AU  - Valk GD
LA  - eng
PT  - Journal Article
PL  - England
TA  - Clin Endocrinol (Oxf)
JT  - Clinical endocrinology
JID - 0346653
RN  - 0 (Blood Glucose)
RN  - 0 (MEN1 protein, human)
RN  - 0 (Proto-Oncogene Proteins)
SB  - IM
MH  - Adult
MH  - Blood Glucose/*genetics/*metabolism
MH  - Female
MH  - Genetic Predisposition to Disease
MH  - Homeostasis
MH  - Humans
MH  - Insulin Resistance/genetics
MH  - Male
MH  - Mutation
MH  - Proto-Oncogene Proteins/*genetics/*metabolism
EDAT- 2011/07/06 06:00
MHDA- 2012/08/14 06:00
CRDT- 2011/07/06 06:00
PHST- 2011/07/06 06:00 [entrez]
PHST- 2011/07/06 06:00 [pubmed]
PHST- 2012/08/14 06:00 [medline]
AID - 10.1111/j.1365-2265.2011.04166.x [doi]
PST - ppublish
SO  - Clin Endocrinol (Oxf). 2012 Jan;76(1):67-71. doi: 
      10.1111/j.1365-2265.2011.04166.x.