Abdominal obesity, particularly excess intraperitoneal fat, is conside
red to play a major role in causing insulin resistance and NIDDM. To d
etermine if NIDDM patients accumulate excess intraperitoneal fat, and
whether this contributes significantly to their insulin resistance, 31
men with mild NIDDM with a wide range of adiposity were compared with
39 nondiabetic, control subjects for insulin sensitivity (measured us
ing euglycemic-hyperinsulinemic clamp technique with [3-H-3]glucose tu
rnover) and total and regional adiposity (assessed by hydrodensitometr
y and by measuring subcutaneous abdominal, intraperitoneal, and retrop
eritoneal fat masses using magnetic resonance imaging [MRI], and trunc
al and peripheral skinfold thicknesses using calipers). MRI analysis r
evealed that intraperitoneal fat was not increased in NIDDM patients c
ompared with control subjects; in both groups it averaged 11% of total
body fat, NIDDM patients, however, had increased truncal-to-periphera
l skinfolds thickness ratios. In NIDDM patients, as in control subject
s, amounts of truncal subcutaneous fat showed a stronger correlation w
ith glucose disposal rate than intraperitoneal or retroperitoneal fat;
however, NIDDM patients were more insulin resistant at every level of
total or regional adiposity. Further, no particular influence of exce
ss intraperitoneal fat on hepatic insulin sensitivity was noted. We co
nclude that NIDDM patients do not have excess intraperitoneal fat, but
that their fat distribution favors more truncal and less peripheral s
ubcutaneous fat. Moreover, for each level of total and regional adipos
ity, NIDDM patients have a heightened state of insulin resistance.