Ej. Mayer-davis et al., Insulin secretion, obesity, and potential behavioral influences: results from the Insulin Resistance Atherosclerosis Study (IRAS), DIABET M R, 17(2), 2001, pp. 137-145
Background This work was conducted to evaluate associations of insulin secr
etion with overall and central obesity, dietary fats, physical activity, an
d alcohol.
Methods A frequently sampled intravenous glucose tolerance test (FSIGT) was
used to assess acute insulin response to glucose (AIR) and insulin sensiti
vity (SI) among adult participants (n = 675 with normal, NGT; n = 332 with
impaired glucose tolerance, IGT) in the Insulin Resistance Atherosclerosis
Study (IRAS). Disposition index (DI) was calculated as the sum of the log-t
ransformed AIR and SI to reflect pancreatic compensation for insulin resist
ance. Obesity was measured as body mass index (kg/m(2), BMI) and central fa
t distribution by waist circumference (cm). Dietary fat intake (total, satu
rated, polyunsaturated, oleic acid), physical activity, and alcohol intake
were assessed by standardized interview.
Results In unadjusted analyses, BMI and waist were each positively correlat
ed with AIR among NGTs (r = 0.26 and 0.23, respectively; p < 0.0001) but co
rrelations were weaker among the IGTs (r = 0.10, NS; r = 0.13, p <0.05 for
BMI and waist, respectively). BMI and waist were inversely correlated with
DI among NGTs (r = -0.13 and -0.20, respectively; p < 0.0001) and among IGT
s (r = -0.20 and -0.19, respectively, p < 0.0001). Dietary fat variables we
re positively related, and alcohol was inversely related, to AIR among NGTs
(p < 0.01) but not among IGTs. With all factors considered simultaneously
in a pooled analysis of IGTs and NGTs, waist, but not BMI, was positively a
ssociated with AIR (p < 0.001) and inversely associated with DI (p < 0.01).
None of the behavioral variables were independently related to either outc
ome.
Conclusion Among non-diabetic patients, central obesity appears to be relat
ed to higher insulin secretion, but to lower capacity of the pancreas to re
spond to the ambient insulin resistance. Copyright (C) 2001 John Wiley & So
ns, Ltd.