title: Shiftwork and higher pancreatic secretion: early detection of an intermediate state of insulin resistance?
abstract: Previous studies have suggested that shiftwork can affect the prevalence of metabolic syndrome. This is thought to be related to disturbance of lipid parameters rather than their effects on glucose metabolism. Several complex mechanisms are suspected to be involved and notably insulin resistance, though the available data are limited. The objective of the present study was to provide further evidence for the effects of shiftwork on glucose and lipid metabolism with a specific focus on insulin resistance. A cross-sectional study has recruited 97 shiftworkers (SWs) (three shifts, 8 h) and 95 strictly day workers (DWs) from the same plant for 2001-2002. Several indices of insulin sensitivity or resistance were calculated, based on formulas of the homeostasis model assessment for insulin resistance (HOMA-IR), the Revised-Quicki, McAuley and Disse indices. The HOMA-β-cell index was used as a reflection of pancreatic secretion. Characteristics of the occupation, habitual diet and lifestyles were recorded. Logistic regression analysis in which pancreatic function or insulin sensitivity was the dependent variable was used to compare alternative models.
  
  
  RESULTS
  SWs were characterized as having significantly higher triglycerides and free fatty acids and normal but lower blood glucose. The risk of a high β-cell activity was increased almost three-fold in SWs. By adjusting for many confounding factors, SWs had significantly lower insulin sensitivity according to several indices, whereas HOMA-IR was not meaningfully different between shift and DWs. Lower insulin sensitivity and a compensatory pancreas response to maintain a normal glucose tolerance may suggest an intermediate state before development of frank insulin resistance in SWs. Early detection of these moderate alterations of the insulin/glucose balance could be important in the prevention of diabetes.
authors.affiliation: UMR 1027: INSERM, University School of Medicine Paul-Sabatier Toulouse III, Toulouse F-31073, France. esquirol.y@chu-toulouse.fr
authors.forename: Yolande
authors.initials: Y
authors.lastname: Esquirol
authors.forename: Vanina
authors.initials: V
authors.lastname: Bongard
authors.forename: Jean
authors.initials: J
authors.lastname: Ferrieres
authors.forename: Helène
authors.initials: H
authors.lastname: Verdier
authors.forename: Bertrand
authors.initials: B
authors.lastname: Perret
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D003430:Cross-Sectional Studies; D006801:Humans; D007328:Insulin / Q000097:blood / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology*; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000378:metabolism*; D020738:Leptin / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology*; D008875:Middle Aged; D012307:Risk Factors; D014940:Work Schedule Tolerance / Q000502:physiology*
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D001786:Blood Glucose; D007328:Insulin; D020738:Leptin