PMID- 22736774
OWN - NLM
STAT- MEDLINE
DCOM- 20121126
LR  - 20221207
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Print)
IS  - 0021-972X (Linking)
VI  - 97
IP  - 9
DP  - 2012 Sep
TI  - Increased serum concentrations of persistent organic pollutants among prediabetic 
      individuals: potential role of altered substrate oxidation patterns.
PG  - E1705-13
LID - 10.1210/jc.2012-1342 [doi]
AB  - CONTEXT: There is a need for a better understanding of the potential role of 
      persistent organic pollutants (POPs) in the pathogenesis of type 2 diabetes. 
      OBJECTIVE: Our objective was to determine the association of serum concentrations 
      of POPs with early signs of type 2 diabetes in regard to glucose and lipid 
      metabolism. RESEARCH DESIGN AND METHODS: In this cross-sectional study, we used 
      recent studies of 148 Danish middle-aged normoglycemic, prediabetic, and diabetic 
      individuals examined by the euglycemic-hyperinsulinemic clamp technique with 
      indirect calorimetry; 66 of these individuals also had an i.v. glucose tolerance 
      test. Concentrations of POPs were analyzed in banked serum from the participants. 
      Associations with basal and insulin-stimulated glucose and lipid metabolism were 
      assessed after adjustment for age, sex, and body fat percentage. RESULTS: 
      Individuals with prediabetes and diabetes had higher serum concentrations of 
      several POPs compared with normoglycemic individuals. In the nondiabetic 
      population, higher POPs levels were associated with elevated fasting plasma 
      glucose concentrations as well as reduced glucose oxidation, elevated lipid 
      oxidation, and elevated serum concentrations of free fatty acids (P < 0.05). We 
      found no associations of POPs with first-phase insulin secretion, hepatic or 
      peripheral insulin sensitivity, or nonoxidative glucose metabolism. CONCLUSIONS: 
      Diabetic and prediabetic individuals have elevated serum concentrations of POPs. 
      In nondiabetic individuals, POPs exposure is related to altered substrate 
      oxidation patterns with lower glucose oxidation and higher lipid oxidation rates. 
      These findings indicate that POPs may affect peripheral glucose metabolism by 
      modifying pathways involved in substrate partitioning rather than decreasing 
      insulin-dependent glucose uptake.
FAU - Faerch, Kristine
AU  - Faerch K
AD  - Steno Diabetes Center, Niels Steensens Vej 2, DK-2820 Gentofte, Denmark. 
      krif@steno.dk
FAU - Hojlund, Kurt
AU  - Hojlund K
FAU - Vind, Birgitte F
AU  - Vind BF
FAU - Vaag, Allan
AU  - Vaag A
FAU - Dalgard, Christine
AU  - Dalgard C
FAU - Nielsen, Flemming
AU  - Nielsen F
FAU - Grandjean, Philippe
AU  - Grandjean P
LA  - eng
GR  - R01 ES013692/ES/NIEHS NIH HHS/United States
GR  - ES013692/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20120626
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
RN  - 0 (Environmental Pollutants)
RN  - 0 (Glycated Hemoglobin A)
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Insulin)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Body Mass Index
MH  - Chromatography, High Pressure Liquid
MH  - Cross-Sectional Studies
MH  - Diabetes Mellitus, Type 2/blood
MH  - Environmental Pollutants/*adverse effects/*blood
MH  - Female
MH  - Glucose/metabolism
MH  - Glucose Clamp Technique
MH  - Glucose Tolerance Test
MH  - Glycated Hemoglobin/analysis
MH  - Humans
MH  - Hypoglycemic Agents/pharmacology
MH  - Insulin/pharmacology
MH  - Insulin Resistance/physiology
MH  - Insulin-Secreting Cells/physiology
MH  - Lipid Metabolism/drug effects/physiology
MH  - Male
MH  - Middle Aged
MH  - Obesity/blood
MH  - Oxidation-Reduction
MH  - Pancreatic Function Tests
MH  - Prediabetic State/*blood
PMC - PMC3431564
EDAT- 2012/06/28 06:00
MHDA- 2012/12/10 06:00
PMCR- 2013/09/01
CRDT- 2012/06/28 06:00
PHST- 2012/06/28 06:00 [entrez]
PHST- 2012/06/28 06:00 [pubmed]
PHST- 2012/12/10 06:00 [medline]
PHST- 2013/09/01 00:00 [pmc-release]
AID - jc.2012-1342 [pii]
AID - 12-1342 [pii]
AID - 10.1210/jc.2012-1342 [doi]
PST - ppublish
SO  - J Clin Endocrinol Metab. 2012 Sep;97(9):E1705-13. doi: 10.1210/jc.2012-1342. Epub 
      2012 Jun 26.