ArticleThe Journal of physiology2016
Hepatic mitochondrial oxidative phosphorylation is normal in obese patients with and without type 2 diabetes.
Article in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 36 citations in OpenAlex.
- Glucagon promotes increased hepatic mitochondrial oxidation and pyruvate carboxylase flux in humans with fatty liver disease.Cell metabolism · 2024Article
- Relationship between serum β-hydroxybutyrate and hepatic fatty acid oxidation in individuals with obesity and NAFLD.American journal of physiology. Endocrinology and metabolism · 2024Article
- Targeting the Metabolic Paradigms in Cancer and Diabetes.Biomedicines · 2024Review
- Impairment of Mitochondrial Respiration in Metabolic Diseases: An Overview.International journal of molecular sciences · 2022Review
- Influence of NAFLD and bariatric surgery on hepatic and adipose tissue mitochondrial biogenesis and respiration.Nature communications · 2022Article
- Atorvastatin impairs liver mitochondrial function in obese Göttingen Minipigs but heart and skeletal muscle are not affected.Scientific reports · 2021Article
- Assessment of mitochondrial function in metabolic dysfunction-associated fatty liver disease using obese mouse models.Zoological research · 2020Article
- Mitochondrial function in liver cells is resistant to perturbations in NADThe Journal of biological chemistry · 2019Article
- Exercise training upregulates SIRT1 to attenuate inflammation and metabolic dysfunction in kidney and liver of diabeticNutrition & metabolism · 2019Article
- α-Linolenic acid supplementation and exercise training reveal independent and additive responses on hepatic lipid accumulation in obese rats.American journal of physiology. Endocrinology and metabolism · 2017Article
- Challenging dogma: is hepatic lipid accumulation in type 2 diabetes due to mitochondrial dysfunction?The Journal of physiology · 2016Article
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11 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
key pointsHepatic insulin resistance in patients with obesity or type 2 diabetes has been suggested to result from hepatic mitochondrial dysfunction. High-resolution respirometry (HRR) can be used to assess oxidative phosphorylation by measuring the mitochondrial oxygen consumption rate in the individual complexes of the mitochondria. By using HRR, the present study demonstrates no difference in hepatic mitochondrial oxidative phosphorylation among subjects with obesity with or without type 2 diabetes and non-obese controls. Furthermore, the amount of mitochondria, assessed by the citrate synthase activity, is not different between the three groups. Together the present findings indicate that hepatic mitochondrial oxidative phosphorylation capacity is not impaired in patients with obesity or type 2 diabetes. ABSTRACT: Obese patients with type 2 diabetes (T2DM) and without type 2 diabetes (OB) are characterized by high hepatic lipid content and hepatic insulin resistance. This may be linked to impaired hepatic mitochondrial oxidative phosphorylation (OXPHOS) capacity. The aim of the present study was to investigate and compare hepatic mitochondrial OXPHOS capacity in T2DM, OB and non-obese controls (CON). Seventeen obese patients (nine OB and eight T2DM) and six CON patients had perioperative liver biopsies taken. Samples were divided into three parts to measure (1) complex I, II and IV linked respiration, (2) citrate synthase (CS) activity and (3) lipid droplet (LD) size and area (% of total tissue area filled by LDs). State 3 respiration of complex I, II and IV and the CS activity did not differ in OB, T2DM and CON. LD size was significantly higher in T2DM compared with CON, and LD area tended (P = 0.10) to be higher in T2DM and OB compared with CON. The present findings indicate that hepatic OXPHOS capacity is not different in patients with markedly different weight and glycaemic control. Furthermore, the results do not support impaired hepatic mitochondrial respiratory capacity playing a major role in the development of obesity-induced type 2 diabetes.
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