Patients with non-insulin-dependent diabetes metlitus (NIDDM) exhibit decreased rates of skeletal muscle insulin-mediated glucose uptake (IMGU). Because IMGU is equal to the product of the arteriovenous glucose difference (AVGΔ) across and blood flow (F) into muscle (IMGU = AVGΔ × F), reduced tissue permeability (AVGΔ) and/or glucose and insulin delivery (F) can potentially lead to decreased IMGU. The components of skeletal muscle IMGU were studied in six obese NIDDM subjects (103 ± 9 kg) and compared with those previously determined in six lean (weight 68 ± 3 kg), and six obese (94 ± 3 kg) with normal glucose tolerance. The insulin dose-response curves for whole body and leg muscle IMGU were constructed using the combined euglycemic clamp and leg balance techniques during sequential insulin infusions (range of serum insulin 130–80,000 pmol/L). In lean, obese, and NIDDM subjects, whole body IMGU, femoral AVGΔ, and leg IMGU increased in a dose-dependent fashion over the range of insulin with an ED50 of 400–500 pmol/L in lean, 1000–1200 pmol/L in obese, and 4000–7000 pmol/L in NIDDM subjects (P < 0.01 lean vs. obese and NIDDM). In lean and obese subjects, maximally effective insulin concentrations increased leg blood flow ∼2-fold from basal with an ED50 of 266 pmol/L and 957 pmol/L, respectively (P < 0.01 lean vs. obese). In contrast, leg F did not increase from the basal value in NIDDM subjects (2.7 ± 0.1 vs. 3.5 ± 0.5 dl/min, NS). In the physiological range of insulin concentrations NIDDM subjects had lower body IMGU, leg F, femoral AVGΔ, and leg IMGU than obese and lean subjects, but at maximally effective insulin concentrations, femoral AVGA did not differ between obese and NIDDM subjects. Thus, 1) both reduced skeletal muscle tissue permeability and blood flow are found in NIDDM subjects and 2) impaired insulin-mediated augmentation of skeletal muscle blood flow in obese NIDDM patients is due to the diabetic state per se and not to the obesity status. Whether reduced skeletal muscle blood flow is the result or the cause of insulin resistance in patients with NIDDM remains to be elucidated.
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Original Articles|
September 01 1992
Impaired Insulin-Mediated Skeletal Muscle Blood Flow in Patients With NIDDM
Markku Laakso;
Markku Laakso
Division of Endocrinology and Metabolism, Department of Medicine, Indiana University School of Medicine
Indianapolis, IN
University of California
San Diego, San Diego, California
Veterans Administration Research Services, Indianapolis
Indiana and San Diego, California
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Steven V Edelman;
Steven V Edelman
Division of Endocrinology and Metabolism, Department of Medicine, Indiana University School of Medicine
Indianapolis, IN
University of California
San Diego, San Diego, California
Veterans Administration Research Services, Indianapolis
Indiana and San Diego, California
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Ginger Brechtel;
Ginger Brechtel
Division of Endocrinology and Metabolism, Department of Medicine, Indiana University School of Medicine
Indianapolis, IN
University of California
San Diego, San Diego, California
Veterans Administration Research Services, Indianapolis
Indiana and San Diego, California
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Alain D Baron
Alain D Baron
Division of Endocrinology and Metabolism, Department of Medicine, Indiana University School of Medicine
Indianapolis, IN
University of California
San Diego, San Diego, California
Veterans Administration Research Services, Indianapolis
Indiana and San Diego, California
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Address correspondence and reprint requests to Alain D. Baron, MD, Division of Endocrinology and Metabolism, Department of Medicine, Indiana University Medical Center, 545 Bamhill Drive, EM 421, Indianapolis, IN 46202-5124.
Diabetes 1992;41(9):1076–1083
Article history
Received:
September 09 1991
Revision Received:
March 30 1992
Accepted:
March 30 1992
PubMed:
1499861
Citation
Markku Laakso, Steven V Edelman, Ginger Brechtel, Alain D Baron; Impaired Insulin-Mediated Skeletal Muscle Blood Flow in Patients With NIDDM. Diabetes 1 September 1992; 41 (9): 1076–1083. https://doi.org/10.2337/diab.41.9.1076
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