| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
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
This article has been cited by other articles:
|
|
 |
|
  S. F. Lowry and S. E. Calvano Challenges for modeling and interpreting the complex biology of severe injury and inflammation J. Leukoc. Biol., March 1, 2008; 83(3): 553 - 557. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. B. O'Leary, C. M. Marchetti, R. K. Krishnan, B. P. Stetzer, F. Gonzalez, and J. P. Kirwan Exercise-induced reversal of insulin resistance in obese elderly is associated with reduced visceral fat J Appl Physiol, May 1, 2006; 100(5): 1584 - 1589. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D Williamson, P Gallagher, M Harber, C Hollon, and S Trappe Mitogen-activated protein kinase (MAPK) pathway activation: effects of age and acute exercise on human skeletal muscle J. Physiol., March 15, 2003; 547(3): 977 - 987. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. D. Longo and C. E. Finch Evolutionary Medicine: From Dwarf Model Systems to Healthy Centenarians? Science, February 28, 2003; 299(5611): 1342 - 1346. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 U. N. Das Is Metabolic Syndrome X an Inflammatory Condition? Experimental Biology and Medicine, December 1, 2002; 227(11): 989 - 997. [Abstract] [Full Text]
|
|
|
|
 |
|
 J. P. Kirwan, S. Hauguel-De Mouzon, J. Lepercq, J.-C. Challier, L. Huston-Presley, J. E. Friedman, S. C. Kalhan, and P. M. Catalano TNF-{alpha} Is a Predictor of Insulin Resistance in Human Pregnancy Diabetes, July 1, 2002; 51(7): 2207 - 2213. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
