Cited by 64Mitochondrial Function and PathologyAdipose Tissue and MetabolismMetabolism, Diabetes, and Cancer

Mitochondrial bioenergetics is not impaired in nonobese subjects with type 2 diabetes mellitus

Chattopadhyay, Mrittika, GuhaThakurta, Ishita, Behera, Prajna, Ranjan, Kumar Rajeev, Khanna, Manoj, Mukhopadhyay, Satinath, Chakrabarti, Sasanka·2011·Metabolism

Abstract

Although mitochondrial dysfunction has been well documented in obese people with type 2 diabetes mellitus, its presence or absence in nonobese subjects with type 2 diabetes mellitus has not been well studied so far. The aim of the present study was to assess the status of mitochondrial oxidative phosphorylation in subcutaneous adipose tissue of nonobese type 2 diabetes mellitus subjects in comparison to control, obese nondiabetic, and obese type 2 diabetes mellitus subjects. Mitochondria were isolated from subcutaneous white adipose tissue obtained from the abdominal region of control, obese nondiabetic, nonobese type 2 diabetes mellitus, and obese type 2 diabetes mellitus subjects. The activities of complex I, I to III, II to III, and IV; transmembrane potential; and inorganic phosphate utilization of mitochondria from different groups were measured. Mitochondrial transmembrane potential, inorganic phosphate utilization, and the activities of respiratory chain complexes were significantly reduced in obese nondiabetic and obese type 2 diabetes mellitus patients compared with those in control subjects. No detectable change in mitochondrial functional parameters was observed in case of nonobese type 2 diabetes mellitus subjects compared with control subjects. Furthermore, a significant difference was noticed in mitochondrial phosphate utilization and activities of respiratory complexes, for example, I, I to III, and II to III, between obese type 2 diabetes mellitus subjects and obese nondiabetic subjects. Obesity modulates mitochondrial dysfunction associated with type 2 diabetes mellitus.

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Registry

Crossref · 10.1016/j.metabol.2011.04.015

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  • In obese type 2 diabetic subjects compared to non-obese diabetics, altered fat acid oxidation and lipid storage, impaired insulin signaling and insulin resistance were associated with significantly lower mitochondrial phosphorylation capacity.

    “Interestingly, a significant role altered fat acid oxidation and lipid storage, impaired insulin signaling and insulin resistance were associated significantly lower mitochondrial phosphorylation capacity in obese type 2 diabetic subjects compared to non-obese diabetics (44), thus strengthening the hypothesis that insulin resistance has a direct role on mitochondrial functional impairment.”

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Authors
Chattopadhyay, M., GuhaThakurta, I., Behera, P., Ranjan, K. R., Khanna, M., Mukhopadhyay, S., & Chakrabarti, S.
Affiliations
Institute of Post Graduate Medical Education and Research (IN)
Venue
Metabolism
Publisher
Elsevier BV
Published
2011-12
Volume
60
Issue
12
Pages
1702-1710
ISSN
0026-0495 (ISSN-L)
OpenAlex
W2074038167
Cited by
64
References
47
Citations by year
2026: 2 · 2025: 2 · 2024: 9 · 2023: 6 · 2022: 3 · 2021: 1 · 2020: 7 · 2019: 7 · 2018: 1 · 2017: 10 · 2016: 2 · 2015: 6 · 2014: 4 · 2013: 2 · 2012: 1
FWCI
1.04
Type
journal article
Language
en
Open access
closed
Locations
  • Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords
type 2 diabetes, mitochondrial dysfunction, mitochondrial bioenergetics, oxidative phosphorylation, subcutaneous white adipose tissue, obesity, respiratory chain complexes, mitochondrial membrane potential
MeSH terms
Adult, Blood Glucose, Diabetes Mellitus, Type 2, Energy Metabolism, Female, Humans, Male, Middle Aged, Mitochondria, NADH, NADPH Oxidoreductases, Obesity, Body Mass Index, Membrane Potential, Mitochondrial

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