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Cited by 107Diabetes, Cardiovascular Risks, and LipoproteinsDiabetes Management and ResearchPancreatic function and diabetes

Impaired postprandial glucose utilization in non-insulin-dependent diabetes mellitus

Kelley, David, Mokan, Marian, Veneman, Thiemo·1994·Metabolism
DOI 10.1016/0026-0495(94)90015-9
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Abstract

The importance of impaired glucose utilization in the pathogenesis of postprandial hyperglycemia in non-insulin-dependent diabetes mellitus (NIDDM) is controversial. Three methods were used to assess glucose utilization following ingestion of a mixed meal in 18 NIDDM and 12 nondiabetic subjects. Dual glucose isotopes were used to determine first-pass splanchnic glucose uptake, suppression of endogenous glucose production, and systemic glucose utilization. Leg balance was used to evaluate skeletal muscle glucose metabolism, and systemic and limb indirect calorimetry were used to assess glucose and lipid oxidation. NIDDM subjects had marked postprandial hyperglycemia as compared with nondiabetics (15.35 +/- 0.72 v 5.83 +/- 0.28 mmol, P < .001), accompanied by lower postprandial insulin (179 +/- 25 v 253 +/- 46 pmol, P < .01) and elevated plasma free fatty acids ([FFA] 569 +/- 34 v 314 +/- 20 mumol/L, P < .001). Cumulative postprandial glucose appearance was nearly twofold greater in NIDDM (82.2 +/- 4.7 v 48.7 +/- 4.9 g.5h, P < .001) due to increased endogenous glucose production (56.4 +/- 4.8 v 24.5 +/- 1.9 g, P < .001), whereas first-pass splanchnic uptake of ingested glucose was normal in NIDDM. Cumulative postprandial glucose utilization in NIDDM, after correction for urinary glucose, was unchanged from postabsorptive rates, a pattern also found for postprandial glucose oxidation. Cumulative leg glucose uptake was somewhat less in NIDDM subjects (123 +/- 18 v 173 +/- 14 mumol/100 mL leg tissue.5 h, P = .06), whereas lactate and alanine net release across the leg were nevertheless twofold greater in NIDDM (P = .04) and accounted for nearly half of the leg glucose metabolism in NIDDM.(ABSTRACT TRUNCATED AT 250 WORDS)

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Crossref · 10.1016/0026-0495(94)90015-9

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  • A reduction in the early insulin response results in a lack of adequate suppression of hepatic glucose production with subsequent post-challenge hyperglycaemia and increased insulin concentrations late in the test.

    “This reduction in the early insulin response results in a lack of adequate suppression of hepatic glucose production with subsequent post challenge hyperglycaemia and increased insulin concentrations late in the test [5, 126].”

    From The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes (2003) · cites this paper as [126]

  • The assessment of whole body RQ as a marker of metabolic flexibility can lead to erroneous conclusions about skeletal muscle metabolism, at least in people with type 2 diabetes.

    “Finally, the assessment of whole body RQ as a marker of metabolic flexibility can lead to erroneous conclusions about skeletal muscle metabolism, at least in people with type 2 diabetes.”

    From Metabolic flexibility and insulin resistance (2008) · cites this paper as [23]

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Authors
Kelley, D., Mokan, M., & Veneman, T.
Affiliations
  • University of Pittsburgh (US)
  • United States Department of Veterans Affairs (US)
ORCID
Kelley, David
Venue
Metabolism
Publisher
Elsevier BV
Published
1994-12
Volume
43
Issue
12
Pages
1549-1557
ISSN
0026-0495 (ISSN-L)
DOI
10.1016/0026-0495(94)90015-9
OpenAlex
W1971128106
Cited by
107
References
41
Citations by year
2026: 1 · 2025: 4 · 2023: 1 · 2022: 2 · 2021: 2 · 2020: 1 · 2019: 4 · 2018: 6 · 2017: 3 · 2015: 1 · 2014: 5 · 2012: 3
FWCI
1.17
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Center for Research Resources (M01-RR00056, M01RR000056)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
type 2 diabetes, postprandial hyperglycemia, glucose utilization, endogenous glucose production, skeletal muscle glucose metabolism, plasma free fatty acids, postprandial insulin, glucose oxidation, mixed meal
MeSH terms
Adult, Analysis of Variance, Blood Glucose, Diabetes Mellitus, Type 2, Eating, Glucagon, Glucose, Humans, Insulin, Lactates, Middle Aged, Oxidation-Reduction, Viscera, Muscle, Skeletal, Lactic Acid, Lipid Metabolism

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