NEFA

Insulin, glucagon, glucose, nonesterified fatty acids (NEFA), and lactate response to oral glucose tolerance test (OGTT, 75 g glucose) and their correlation with mean blood pressure (BP), were studied in 10 normal subjects (N), 25 subjects with abdominal obesity (O), and 9 subjects with abdominal obesity and IGT or non-insulin-dependent diabetes (OD). O and OD patients, as compared to N subjects, showed increased fasting NEFA, lactate, insulin, and glucagon. NEFA area and insulin total and incremental areas were increased in O and OD (P<0.001 in all instances). Glucagon total area was increased only in OD (P<0.01). Lactate total area was increased in O (P<0.001) and in OD (P<0.01), while lactate incremental area was diminished in O and, even more, in OD subjects (P<0.001 in both instances) and was inversely correlated with the basal level (P<0.001). In all subjects as a whole, increase in NEFA area was weakly correlated with total and incremental insulinemic areas (P<0.05) and more strongly correlated with glucagon and lactate areas (P<0.01). Conversely, the incremental area of lactate was negatively correlated with total insulin (P<0.05), NEFA (P<0.05), and glucagon (P<0.001) areas. BP was increased in O (103.62 ± 2.37) and, even more, in OD (109.41 ± 5.22) compared to N (92.55 ± 0.94 mm Hg), with P<0.01, and was correlated with fasting insulin (P<0.01) and glucose (P<0.05) and, even more, with total (P<0.001) and incremental (P<0.01) insulin areas and NEFA area (P<0.001). Conversely, BP was negatively correlated with incremental lactate area (P<0.01) (similarly to insulin and NEFA area). Our data would suggest that in O and OD patients, insulin resistance is associated with elevated NEFA, insulin and glucagon as well as with high BP. Since NEFA are inhibitors of Na,K-ATPase, they could contribute to elevate BP through the repression of this enzyme (which we have shown previously to be reduced in adipose tissue of obese subjects and correlated negatively with BP).