CoChat
Sign Up
Cited by 119Metabolism, Diabetes, and CancerDiabetes, Cardiovascular Risks, and LipoproteinsAdipokines, Inflammation, and Metabolic Diseases

The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

Insulin-induced hexokinase II expression is reduced in obesity and NIDDM.

Pendergrass, M, Koval, J, Vogt, C, Yki-Jarvinen, H, Iozzo, P, Pipek, R, Ardehali, H, Printz, R, Granner, D, DeFronzo, R A, Mandarino, L J·1998·Diabetes
DOI 10.2337/diabetes.47.3.387
Open this paper in CoChat — free account

Abstract

NIDDM and obesity are characterized by decreased insulin-stimulated glucose uptake in muscle. It has been suggested that impaired glucose phosphorylation to glucose-6-phosphate, catalyzed in muscle by hexokinase (HK)II, may contribute to this insulin resistance. Insulin is known to increase HKII mRNA, protein, and activity in lean nondiabetic individuals. The purpose of this study was to determine whether defects in insulin-stimulated HKII expression and activity could contribute to the insulin resistance of obesity and NIDDM. Fifteen lean nondiabetic control subjects, 17 obese nondiabetic subjects, and 14 obese NIDDM patients were studied. Percutaneous muscle biopsies of the vastus lateralis were performed in conjunction with leg balance and local indirect calorimetry measurements before and at the end of a 3-h euglycemic-hyperinsulinemic clamp (40 or 240 mU x min(-1) x m[-2]). Leg glucose uptake in response to the 40-mU insulin infusion was higher in the lean control subjects (2.53 +/- 0.35 micromol x min(-1) per x 100 ml leg vol) than in obese (1.46 +/- 0.50) or NIDDM (0.53 +/- 0.25, P < 0.05) patients. In response to 240 mU insulin, leg glucose uptake was similar in all of the groups. In response to 40 mU insulin, HKII mRNA in lean control subjects was increased 1.48 +/- 0.18-fold (P < 0.05) but failed to increase significantly in the obese (1.12 +/- 0.24) or NIDDM (1.14 +/- 0.18) groups. In response to 240 mU insulin, HKII mRNA was increased in all groups (control subjects 1.48 +/- 0.18, P < 0.05 vs. basal, obese 1.30 +/- 0.16, P < 0.05, and NIDDM 1.25 +/- 0.14, P < 0.05). Under basal conditions, HKI and HKII activities did not differ significantly between groups. Neither the 40 mU nor the 240 mU insulin infusion affected HK activity. Total HKII activity was reduced in the obese subjects (4.33 +/- 0.08 pmol x min(-1) x g(-1) muscle protein) relative to the lean control subjects (5.00 +/- 0.08, P < 0.05). There was a further reduction in the diabetic patients (3.10 +/- 0.10, P < 0.01 vs. the control subjects, P < 0.01 vs. the obese subjects). Resistance to insulin's metabolic effects extends to its ability to induce HKII expression in obesity and NIDDM.

Overview

Integrity signals

Registry

Crossref · 10.2337/diabetes.47.3.387

Cites

11 of 11 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Cited by

Sorted by citations

See all 119

Related

See all

Metadata

Authors
Pendergrass, M., Koval, J., Vogt, C., Yki-Jarvinen, H., Iozzo, P., Pipek, R., Ardehali, H., Printz, R., Granner, D., DeFronzo, R. A., & Mandarino, L. J.
Affiliations
  • The University of Texas at San Antonio Health Science Center (US)
  • Department of Medicine, University of Texas Health Science Center at San Antonio, 78284-7886, USA.
ORCID
Venue
Diabetes
Publisher
American Diabetes Association
Published
1998-03-01
Volume
47
Issue
3
Pages
387-394
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diabetes.47.3.387
OpenAlex
W2109297349
Cited by
119
References
11
Citations by year
2025: 1 · 2024: 2 · 2023: 1 · 2022: 5 · 2021: 2 · 2018: 6 · 2017: 4 · 2016: 3 · 2015: 3 · 2014: 6 · 2013: 4 · 2012: 3
FWCI
2.80
Type
journal article
Language
en
Open access
closed
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Diabetes and Digestive and Kidney Diseases (DK47936, DK 20593, DK 24092, R01DK047936)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
Keywords
hexokinase 2, insulin resistance, obesity, type 2 diabetes, skeletal muscle glucose uptake, glucose phosphorylation, hyperinsulinemic-euglycemic clamp, vastus lateralis, muscle glucose metabolism, indirect calorimetry
MeSH terms
Adult, Biopsy, Diabetes Mellitus, Type 2, Dose-Response Relationship, Drug, Female, Glucose, Glycogen Synthase, Hexokinase, Humans, Infusions, Intravenous, Insulin, Leg, Male, Obesity, Regional Blood Flow, RNA, Messenger, Glucose Clamp Technique, Cohort Studies, Gene Expression Regulation, Enzymologic, Muscle, Skeletal

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review