(Hypertension. 1995;26:186-192.)
© 1995 American Heart Association, Inc.
Articles |
Glucose Metabolism in Abdominally Obese Hypertensive and Normotensive Subjects
From the Department of Medicine and the Clinical Research Center, Medical College of Wisconsin, Milwaukee, and the Division of Clinical Pharmacology, Departments of Pharmacology and Medicine, Medical University of South Carolina, Charleston.
Correspondence to Ahmed H. Kissebah, MD, PhD, Department of Medicine, Division of Endocrinology, Metabolism, and Clinical Nutrition, Froedtert Memorial Lutheran Hospital, 9200 W Wisconsin Ave, Milwaukee, WI 53226.
Abstract To determine whether the combination of obesity and hypertension results in additive defects in oxidative and nonoxidative glucose metabolism and the association of these changes with altered hemodynamic actions of insulin, we studied 11 abdominally obese hypertensive, 6 abdominally obese normotensive, and 7 lean normotensive nondiabetic subjects. Endogenous glucose production and glucose metabolized were calculated from a euglycemic clamp at 72 and 287 pmol insulin/m2 per minute. Glucose metabolized divided by insulin was lower at 72 pmol/m2 per minute in both obese groups than in lean normotensive subjects, at 148±14, 144±33, and 373±69 (µmol/m2 per minute)/(pmol/L), respectively (P<.01). Similar results were obtained during the higher insulin dose. Nonoxidative and oxidative glucose disposals by indirect calorimetry were lower in both abdominally obese groups (P<.05). Hepatic glucose production was completely suppressed in lean subjects at the lower insulin dose and in all three groups at the higher insulin dose. Hemodynamic responses during the clamp were not significantly different among the three groups. Abdominal obesity is associated with defects in insulin-regulated oxidative and nonoxidative glucose disposal as well as in insulin suppression of hepatic glucose production. Mild hypertension does not exacerbate these defects. Whereas the global impairment in glucose metabolism suggests the presence of an early defect or defects, including reduced tissue perfusion, systemic and regional hemodynamic responses to insulin were not altered. These findings do not support a direct role for insulin resistance in the pathogenesis of the hypertension associated with abdominal obesity.
Key Words: obesity • glucose clamp technique • glucose • hemodynamics • hypertension, obesity • insulin
This article has been cited by other articles:
 |
|
 |
|
  V. Vu, W. Kim, X. Fang, Y.-T. Liu, A. Xu, and G. Sweeney Coculture with Primary Visceral Rat Adipocytes from Control But Not Streptozotocin-Induced Diabetic Animals Increases Glucose Uptake in Rat Skeletal Muscle Cells: Role of Adiponectin Endocrinology, September 1, 2007; 148(9): 4411 - 4419. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Pitombo, E. P Araujo, C. T De Souza, J. C Pareja, B. Geloneze, and L. A Velloso Amelioration of diet-induced diabetes mellitus by removal of visceral fat J. Endocrinol., December 1, 2006; 191(3): 699 - 706. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Kishino, T. Ito, K. Fujita, and Y. Kiuchi A Mixture of the Salacia reticulata (Kotala himbutu) Aqueous Extract and Cyclodextrin Reduces the Accumulation of Visceral Fat Mass in Mice and Rats with High-Fat Diet-Induced Obesity J. Nutr., February 1, 2006; 136(2): 433 - 439. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. C. Woods, K. Gotoh, and D. J. Clegg Gender Differences in the Control of Energy Homeostasis Experimental Biology and Medicine, November 1, 2003; 228(10): 1175 - 1180. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. Gabriely, X. H. Ma, X. M. Yang, G. Atzmon, M. W. Rajala, A. H. Berg, P. Scherer, L. Rossetti, and N. Barzilai Removal of Visceral Fat Prevents Insulin Resistance and Glucose Intolerance of Aging: An Adipokine-Mediated Process? Diabetes, October 1, 2002; 51(10): 2951 - 2958. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Gupta, J. A. Cases, L. She, X.-H. Ma, X.-M. Yang, M. Hu, J. Wu, L. Rossetti, and N. Barzilai Ability of insulin to modulate hepatic glucose production in aging rats is impaired by fat accumulation Am J Physiol Endocrinol Metab, June 1, 2000; 278(6): E985 - E991. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Laine, M. J. Knuuti, U. Ruotsalainen, T. Utriainen, V. Oikonen, M. Raitakari, M. Luotolahti, O. Kirvela, P. Vicini, C. Cobelli, et al. Preserved Relative Dispersion but Blunted Stimulation of Mean Flow, Absolute Dispersion, and Blood Volume by Insulin in Skeletal Muscle of Patients With Essential Hypertension Circulation, June 2, 1998; 97(21): 2146 - 2153. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y.-J. Liu, Y. Nakagawa, and T. Ohzeki Gene Expression of 11ß-Hydroxysteroid Dehydrogenase Type 1 and Type 2 in the Kidneys of Insulin-Dependent Diabetic Rats Hypertension, March 1, 1998; 31(3): 885 - 889. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. M.I. Hennes, I. M. O'Shaughnessy, T. M. Kelly, P. LaBelle, B. M. Egan, and A. H. Kissebah Insulin-Resistant Lipolysis in Abdominally Obese Hypertensive Individuals: Role of the Renin-Angiotensin System Hypertension, July 1, 1996; 28(1): 120 - 126. [Abstract] [Full Text]
|
|
|
|
|
|
B. M. Egan, M. M.I. Hennes, K. T. Stepniakowski, I. M. O'Shaughnessy, A. H. Kissebah, and T. L. Goodfriend Obesity Hypertension Is Related More to Insulin's Fatty Acid Than Glucose Action Hypertension, March 1, 1996; 27(3): 723 - 728. [Abstract] [Full Text]
|
|
|
|
|
|
R. K. Davda, K. T. Stepniakowski, G. Lu, M. E. Ullian, T. L. Goodfriend, and B. M. Egan Oleic Acid Inhibits Endothelial Nitric Oxide Synthase by a Protein Kinase C-Independent Mechanism Hypertension, November 1, 1995; 26(5): 764 - 770. [Abstract] [Full Text]
|
|