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production during hyperglycemia and hyperinsulinemia
1 Departments of Reproductive Biology and 2 Nutrition, Case Western Reserve University School of Medicine at MetroHealth Medical Center, Cleveland, Ohio 44109; 3 Noll Physiological Research Center, Pennsylvania State University, University Park, Pennsylvania 16802; and 4 Nutrition, Metabolism, and Exercise Division, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72114
Changes in tumor necrosis
factor-
(TNF-) may provide a mechanism to explain impaired
glucose metabolism with advancing age. Hyperglycemic clamps (180 min,
10 mM) were performed on seven older [67 ± 2 yr; body mass index
(BMI) 24.7 ± 1.0 kg/m2] and seven younger (22 ± 1 yr; BMI 21.8 ± 1.3 kg/m2) healthy sedentary
males with normal glucose tolerance. TNF- production at basal and at
the end of 180 min of hyperglycemia and hyperinsulinemia was measured
ex vivo from lipopolysaccharide-stimulated (1 ng/ml) peripheral blood
mononuclear cells. Plasma glucose, insulin, and C-peptide levels were
similar in both groups at basal and during the last 30 min of the
hyperglycemic clamp. Glucose infusion rates were lower
(P < 0.004) in the older group compared with the
young, indicating decreased insulin action among the older subjects.
Basal TNF- secretion was similar in older and younger subjects.
TNF- was suppressed (P < 0.02) in the younger group
(230 ± 46 vs. 126 ± 49 pg/ml; basal vs. clamp) but not in the older group (153 ± 37 vs. 182 ± 42 pg/ml), with
significant group differences in response (P < 0.05).
A significant correlation was observed between the level of suppression
in TNF- production and insulin action (Kendall's rank, 
= 0.40, P < 0.05). Furthermore, the TNF- response
during the clamp was related to fat mass (r = 0.88, P < 0.001) and abdominal fat (r = 0.81, P < 0.003). In conclusion, these findings
suggest a possible mechanism by which TNF- may modulate glucose
metabolism in younger people. Aging and modest increases in adiposity
prevent the "normal" suppression of TNF- production after a
sustained postprandial-like hyperglycemic-hyperinsulinemic stimulus,
which may contribute in part to the decline in insulin sensitivity in
older men.
insulin resistance; obesity; diabetes; abdominal adiposity
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