Contribution of abnormal muscle and liver glucose metabolism to postprandial hyperglycemia in NIDDM

Journal Article · Wed Oct 31 23:00:00 EST 1990 · Diabetes; (USA)

DOI:https://doi.org/10.2337/diabetes.39.11.1381· OSTI ID:6274848

Mitrakou, A; Kelley, D; Veneman, T; Jenssen, T; Pangburn, T; Reilly, J; Gerich, J ^[1]

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1. Univ. of Pittsburgh School of Medicine, PA (USA)

To assess the role of muscle and liver in the pathogenesis of postprandial hyperglycemia in non-insulin-dependent diabetes mellitus (NIDDM), we administered an oral glucose load enriched with (14C)glucose to 10 NIDDM subjects and 10 age- and weight-matched nondiabetic volunteers and compared muscle glucose disposal by measuring forearm balance of glucose, lactate, alanine, O2, and CO2. In addition, we used the dual-lable isotope method to compare overall rates of glucose appearance (Ra) and disappearance (Rd), suppression of endogenous glucose output, and splanchnic glucose sequestration. During the initial 1-1.5 h after glucose ingestion, plasma glucose increased by approximately 8 mM in NIDDM vs. approximately 3 mM in nondiabetic subjects (P less than 0.01); overall glucose Ra was nearly 11 g greater in NIDDM than nondiabetic subjects, but glucose Rd was not significantly different in NIDDM and nondiabetic subjects. The greater overall glucose Ra of NIDDM subjects was due to 6.8 g greater endogenous glucose output (13.7 +/- 1.1 vs. 6.8 +/- 1.0 g, P less than 0.01) and 3.8 g less oral glucose splanchnic sequestration of the oral load (31.4 +/- 1.5 vs. 27.5 +/- 0.9 g, P less than 0.05). Although glucose taken up by muscle was not significantly different in NIDDM and nondiabetic subjects (39.3 +/- 3.5 vs. 41.0 +/- 2.5 g/5 h), a greater amount of the glucose taken up by muscle in NIDDM was released as lactate and alanine (11.7 +/- 1.0 vs. 5.2 +/- 0.3 g in nondiabetic subjects, P less than 0.01), and less was stored (11.7 +/- 1.3 vs. 16.9 +/- 1.5 g, P less than 0.05). We conclude that increased systemic glucose delivery, due primarily to reduced suppression of endogenous hepatic glucose output and, to a lesser extent, reduced splanchnic glucose sequestration, is the predominant factor responsible for postprandial hyperglycemia in NIDDM.

• OSTI ID: 6274848
• Journal Information: Diabetes; (USA), Journal Name: Diabetes; (USA) Vol. 39:11; ISSN 0012-1797; ISSN DIAEA
• Country of Publication: United States
• Language: English

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59 BASIC BIOLOGICAL SCIENCES
ALANINES
ALDEHYDES
AMINO ACIDS
BODY
CARBOHYDRATES
CARBON 14 COMPOUNDS
CARBON COMPOUNDS
CARBON DIOXIDE
CARBON OXIDES
CARBOXYLIC ACID SALTS
CARBOXYLIC ACIDS
CHALCOGENIDES
DIABETES MELLITUS
DIGESTIVE SYSTEM
DISEASES
ELEMENTS
ENDOCRINE DISEASES
GLANDS
GLUCOSE
HEXOSES
HYPERGLYCEMIA
ISOTOPE APPLICATIONS
LABELLED COMPOUNDS
LACTATES
LIVER
METABOLIC DISEASES
METABOLISM
MONOSACCHARIDES
MUSCLES
NONMETALS
ORGANIC ACIDS
ORGANIC COMPOUNDS
ORGANS
OXIDES
OXYGEN
OXYGEN COMPOUNDS
PATHOGENESIS
SACCHARIDES
TRACER TECHNIQUES