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Cited by 535Adipokines, Inflammation, and Metabolic DiseasesPancreatic function and diabetesAdipose Tissue and Metabolism

The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.

Tumor necrosis factor impairs insulin action on peripheral glucose disposal and hepatic glucose output.

Lang, C H, Dobrescu, C, Bagby, G J·1992·Endocrinology
DOI 10.1210/endo.130.1.1727716
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Abstract

The present study examined whether a prolonged infusion of tumor necrosis factor (TNF) into rats could sustain the increased rate of whole body glucose metabolism observed with short term exposure, and whether TNF produced hepatic or peripheral insulin resistance. Basal glucose metabolism was determined with the use of [3-3H]glucose 18 h after initiating a constant infusion of recombinant human TNF (1 microgram/kg.h). Thereafter, a two-step euglycemic hyperinsulinemic clamp was performed to determine whether TNF impaired insulin action. The overnight infusion of TNF minimally elevated plasma glucose concentrations (17%), but produced large increases in the whole body rate of glucose production and utilization (133%). Under hyperinsulinemic conditions, the glucose infusion rate necessary to maintain euglycemia was 30% lower in TNF-treated rats, indicating an insulin-resistant condition. This resulted from an impaired ability of insulin to both suppress hepatic glucose production and stimulate peripheral glucose utilization in TNF-infused animals. A second series of experiments was performed, using the in vivo tracer [U-14C]2-deoxyglucose technique, to elucidate which tissues were responsible for the TNF-induced increase in basal (no exogenous insulin) glucose disposal and peripheral insulin resistance. Under basal conditions, TNF increased glucose uptake by various muscles (gastrocnemius, heart, and diaphragm) as well as nonmuscle tissues (liver, lung, spleen, gut, skin and fat). Because of their relatively large mass and/or high rate of glucose uptake, the increased uptake by skin (25%), intestine (24%), muscle (23%), and liver (15%) accounted for the majority of the TNF-induced increment in whole body glucose disposal. Under euglycemic hyperinsulinemic conditions, the increment in glucose uptake by muscle and skin (85%) accounted for the majority of the glucose disposal in control rats. However, in TNF-infused animals, hyperinsulinemia failed to increase glucose uptake by skin and blunted the insulin-mediated increase in muscle by 73%. These results suggest that sustained elevations of TNF during chronic therapy and prolonged production of TNF by patients and experimental animals with malignancies or infectious diseases may be an important mechanism for the enhanced glucose flux as well as the insulin resistance seen in these conditions.

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Crossref · 10.1210/endo.130.1.1727716

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Metadata

Authors
Lang, C. H., Dobrescu, C., & Bagby, G. J.
Affiliations
Louisiana State University (US)
ORCID
Lang, C H
Venue
Endocrinology
Publisher
The Endocrine Society
Published
1992-01
Volume
130
Issue
1
Pages
43-52
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
DOI
10.1210/endo.130.1.1727716
OpenAlex
W2067057146
Cited by
535
References
31
Citations by year
2026: 3 · 2025: 7 · 2024: 7 · 2023: 2 · 2022: 9 · 2021: 10 · 2020: 8 · 2019: 7 · 2018: 9 · 2017: 13 · 2016: 15 · 2015: 11 · 2014: 18 · 2013: 24 · 2012: 17
FWCI
9.94
Type
journal article
Language
en
Open access
closed
Locations
  • Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5p01gm032654-10)
  • National Institute of General Medical Sciences (GM 32654, GM 38032)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
  • Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
Keywords
TNF-α, insulin resistance, hepatic glucose production, hyperinsulinemic-euglycemic clamp, glucose uptake, muscle glucose uptake, whole-body glucose metabolism
MeSH terms
Animals, Glucose, Insulin Antagonists, Insulin Resistance, Liver, Male, Rats, Inbred Strains, Tumor Necrosis Factor-alpha, Rats

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