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Cited by 220Pancreatic function and diabetesMitochondrial Function and PathologyAdipose Tissue and Metabolism

The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.

Uncoupling Protein 2 Knockout Mice Have Enhanced Insulin Secretory Capacity After a High-Fat Diet

Joseph, Jamie W., Koshkin, Vasilij, Zhang, Chen-Yu, Wang, Jing, Lowell, Bradford B., Chan, Catherine B., Wheeler, Michael B.·2002·Diabetes
DOI 10.2337/diabetes.51.11.3211
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Abstract

Uncoupling protein 2 (UCP2) may act as an important regulator of insulin secretion. In this study, β-cell function in UCP2-deficient mice was examined after a 45% high-fat diet (HFD) to assess its role during the development of diet-induced type 2 diabetes. HFD-fed UCP2 (−/−) mice have lower fasting blood glucose and elevated insulin levels when compared with wild-type (WT) mice. UCP2 (−/−) mice also have enhanced β-cell glucose sensitivity compared with WT mice after HFD, a result that is due in part to the deterioration of glucose responsiveness in WT mice. HFD-fed UCP2 (−/−) mice have increased insulin secretory capacity as a result of increased pancreatic β-cell mass and insulin content per islet. Islets from WT mice exposed to 0.5 mmol/l palmitate for 48 h have significantly reduced mitochondrial membrane potential, ATP concentrations, and glucose responsiveness compared with UCP2 (−/−) islets, suggesting that elevated UCP2 in WT mice increases proton leak and decreases mitochondrial ATP production. Highly increased carnitine palmitoyl transferase-1 gene expression in UCP2 (−/−) mice is suggestive of enhanced fatty acid oxidizing capacity, particularly after HFD stress. These results further establish UCP2 as a component in glucose sensing and suggest a possible new aspect of UCP2 function during the progression of type 2 diabetes.

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Metadata

Authors
Joseph, J. W., Koshkin, V., Zhang, C.-Y., Wang, J., Lowell, B. B., Chan, C. B., & Wheeler, M. B.
Affiliations
  • University of Toronto (CA)
  • Division of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts
  • Beth Israel Deaconess Medical Center (US)
  • University of Prince Edward Island (CA)
ORCID
Venue
Diabetes
Publisher
American Diabetes Association
Published
2002-11-01
Volume
51
Issue
11
Pages
3211-3219
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diabetes.51.11.3211
OpenAlex
W2161371876
Cited by
220
References
50
Citations by year
2026: 1 · 2025: 1 · 2024: 5 · 2023: 2 · 2022: 3 · 2021: 5 · 2020: 3 · 2019: 4 · 2018: 3 · 2017: 7 · 2016: 5 · 2015: 14 · 2014: 6 · 2013: 7 · 2012: 17
FWCI
11.74
Type
journal article
Language
en
Open access
closed
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Diabetes and Digestive and Kidney Diseases (R37DK053477)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
Keywords
UCP2, UCP2 knockout mice, insulin secretion, beta-cell function, high-fat diet, type 2 diabetes, beta-cell glucose sensitivity, beta-cell mass, mitochondrial membrane potential, mitochondrial ATP production, proton leak, carnitine palmitoyltransferase 1, fatty acid oxidation, glucose detection
MeSH terms
Uncoupling Protein 2, Insulin Secretion, Animals, Base Sequence, Blood Glucose, Diabetes Mellitus, Type 2, Dietary Fats, Disease Models, Animal, Fatty Acids, Nonesterified, Glucagon, Insulin, Ion Channels, Proteins, Triglycerides, Weight Gain, DNA Primers, Mice, Knockout, Mitochondrial Proteins, Membrane Transport Proteins, Mice

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