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Insulin-Mediated Hemodynamic Changes Are Impaired in Muscle of Zucker Obese Rats


Wallis, MG and Wheatley, C and Rattigan, S and Barrett, EJ and Clark, ADH and Clark, MG, Insulin-Mediated Hemodynamic Changes Are Impaired in Muscle of Zucker Obese Rats, Diabetes, 51, (12) pp. 3492-3498. ISSN 0012-1797 (2002) [Refereed Article]

DOI: doi:10.2337/diabetes.51.12.3492


Insulin-mediated hemodynamic effects in muscle were assessed in relation to insulin resistance in obese and lean Zucker rats. Whole-body glucose infusion rate (GIR), femoral blood flow (FBF), hindleg glucose extraction (HGE), hindleg glucose uptake (HGU), 2-deoxyglucose (DG) uptake into muscles of the lower leg (R g), and metabolism of infused 1-methylxanthine (1- MX) to measure capillary recruitment were determined for isogylcemic (4.8 ± 0.2 mmol/l, lean; 11.7 ± 0.6 mmol/l, obese) insulin-clamped (20 mU · min -1 · kg -1 × 2 h) and saline-infused control anesthetized age-matched (20 weeks) lean and obese animals. Obese rats (445 ± 5 g) were less responsive to insulin than lean animals (322 ± 4 g) for GIR (7.7 ± 1.4 vs. 22.2 ± 1.1 mg · min -1 · kg -1, respectively), and when compared with saline-infused controls there was no increase due to insulin by obese rats in FBF, HGE, HGU, and R g of soleus, plantaris, red gastrocnemius, white gastrocnemius, extensor digitorum longus (EDL), or tibialis muscles. In contrast, lean animals showed marked increases due to insulin in FBF (5.3-fold), HGE (5-fold), HGU (8-fold), and R g (∼5.6-fold). Basal (saline) hindleg 1-MX metabolism was 1.5-fold higher in lean than in obese Zucker rats, and insulin increased in only that of the lean. Hindleg 1-MX metabolism in the obese decreased slightly in response to insulin, thus postinsulin lean was 2.6-fold that of the postinsulin obese. We conclude that muscle insulin resistance of obese Zucker rats is accompanied by impaired hemodynamic responses to insulin, including capillary recruitment and FBF.

Item Details

Item Type:Refereed Article
Research Division:Biomedical and Clinical Sciences
Research Group:Clinical sciences
Research Field:Endocrinology
Objective Division:Health
Objective Group:Clinical health
Objective Field:Clinical health not elsewhere classified
UTAS Author:Wallis, MG (Ms Michelle Gaye Wallis)
UTAS Author:Wheatley, C (Ms Catherine Wheatley)
UTAS Author:Rattigan, S (Professor Stephen Rattigan)
UTAS Author:Clark, ADH (Mr Andrew Clark)
UTAS Author:Clark, MG (Professor Michael Clark)
ID Code:24661
Year Published:2002
Web of Science® Times Cited:112
Deposited By:Biochemistry
Deposited On:2002-08-01
Last Modified:2003-04-11

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