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August 15, 1997Journal of Clinical InvestigationOpen Access

Intact insulin stimulation of skeletal muscle blood flow, its heterogeneity and redistribution, but not of glucose uptake in non-insulin-dependent diabetes mellitus.

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Why the study?

Does insulin stimulation improve skeletal muscle blood flow and glucose uptake in men with NIDDM compared to normal men?

Population

17 men, comprising 10 with non-insulin-dependent diabetes mellitus and 7 matched normal men.

Comparison

Normoglycemic hyperinsulinemic conditions vs Basal conditions and matched normal men

Design

Case-control

Authors

TUTapio UtriainenUniversity of HelsinkiPNPirjo NuutilaCardiac ImagingTTTuomo TakalaUniversity of Eastern Finland

Discussion

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Implication

Preserved insulin-stimulated muscle blood flow in NIDDM; leaves open cellular uptake defects as primary driver in case-control data.

Key Points

  • To determine whether defects in insulin-stimulated skeletal muscle blood flow, flow dispersion, or flow-glucose uptake coupling contribute to insulin resistance in non-insulin-dependent diabetes mellitus (NIDDM).
  • Evaluated 10 men with NIDDM (HbA1c 8.1±0.5%, age 43±2 yr, BMI 27.3±0.7 kg/m2) and 7 matched healthy control men under normoglycemic hyperinsulinemic clamp conditions.
  • Used positron emission tomography (PET) with [15O]H2O and [18F]-2-deoxy-D-glucose combined with a Bayesian iterative reconstruction algorithm to quantify mean muscle blood flow, spatial flow heterogeneity, and local glucose uptake.
  • Whole-body glucose uptake (35±3 vs. 44±3 µmol/kg body weight·min, P < 0.05) and femoral muscle glucose uptake (71±6 vs. 96±7 µmol/kg muscle·min, P < 0.02) were significantly reduced in men with NIDDM compared to controls.
  • Insulin stimulated mean muscle blood flow similarly in NIDDM (1.9±0.3 to 2.8±0.4 ml/100 g muscle·min, P < 0.01) and controls (2.3±0.3 to 3.0±0.3 ml/100 g muscle·min, P < 0.02).
  • Insulin increased absolute flow dispersion and successfully colocalized blood flow with regions of glucose uptake in both groups, showing intact vascular recruitment in NIDDM.

Structured PICO

Does insulin stimulation improve skeletal muscle blood flow and glucose uptake in men with NIDDM compared to normal men?

P
Population
17 men, comprising 10 with non-insulin-dependent diabetes mellitus (NIDDM) (mean age 43+/-2 yr, BMI 27.3+/-0.7 kg/m2, HbA1c 8.1+/-0.5%) and 7 matched normal men.
I
Intervention
Normoglycemic hyperinsulinemic conditions (insulin stimulation)
C
Comparator
Basal conditions and matched normal men
O
Outcome
Mean muscle blood flow, flow heterogeneity, and their relationship to glucose uptake measured by positron emission tomographysurrogate

Insulin increases skeletal muscle blood flow and redirects flow to areas of glucose uptake similarly in NIDDM and normal men, suggesting muscle insulin resistance in NIDDM is due to impaired cellular glucose uptake rather than vascular defects.

Cite This Study

Utriainen et al. (1997) studied this question.

synapsesocial.com/papers/6a82631bf10a9fcdd646ce6bhttps://doi.org/10.1172/jci119591
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Evidence for Dissociation of Insulin Stimulation of Blood Flow and Glucose Uptake in Human Skeletal Muscle: Studies Using [15O]H2O, [18F]fluoro-2-deoxy- D -glucose, and Positron Emission Tomography1996 · 61 citations
  2. 2Impaired Insulin-Mediated Skeletal Muscle Blood Flow in Patients With NIDDM1992 · 458 citations
  3. 3Insulin-mediated skeletal muscle vasodilation is nitric oxide dependent. A novel action of insulin to increase nitric oxide release.1994 · 1,225 citations
  4. 4Glucose-free fatty acid cycle operates in human heart and skeletal muscle in vivo.1992 · 316 citations
  5. 5Contribution of Impaired Muscle Glucose Clearance to Reduced Postabsorptive Systemic Glucose Clearance in NIDDM1990 · 40 citations