Lund 2016 J Physiol

From Bioblast
Jump to: navigation, search
Publications in the MiPMap
Lund MT, Kristensen M, Hansen M, Tveskov L, Floyd AK, Støckel M, Vainer B, Poulsen SS, Helge JW, Prats C, Dela F (2016) Hepatic mitochondrial oxidative phosphorylation is normal in obese patients with and without type 2 diabetes. J Physiol 594:4351-8.

» PMID: 27060482 Open Access

Lund MT, Kristensen M, Hansen M, Tveskov L, Floyd AK, Stoeckel M, Vainer B, Poulsen SS, Helge JW, Prats C, Dela F (2016) J Physiol

Abstract: Obese patients with (T2DM) and without (OB) type 2 diabetes 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 in 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 glycemic 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.

This article is protected by copyright. All rights reserved.


O2k-Network Lab: DK Copenhagen Dela F, DK Copenhagen Larsen S


Labels: MiParea: Respiration, Patients  Pathology: Diabetes, Obesity 

Organism: Human  Tissue;cell: Liver  Preparation: Permeabilized tissue  Enzyme: Complex IV;cytochrome c oxidase 

Coupling state: LEAK, OXPHOS, ET  Pathway: F, N, S, CIV, NS, ROX  HRR: Oxygraph-2k 

2016-06