Hepatic mitochondrial oxidative phosphorylation is normal in obese patients with and without type 2 diabetes.
Michael Taulo LundMarianne KristensenMerethe HansenLouise TveskovAndrea Karen FloydMikael StøckelBen VainerSteen Seier PoulsenJørn Wulff HelgeClara PratsFlemming DelaPublished in: The Journal of physiology (2017)
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.
Keyphrases
- type diabetes
- obese patients
- glycemic control
- insulin resistance
- bariatric surgery
- weight loss
- metabolic syndrome
- oxidative stress
- adipose tissue
- roux en y gastric bypass
- gastric bypass
- cardiovascular disease
- end stage renal disease
- chronic kidney disease
- patients undergoing
- physical activity
- high fat diet
- single cell
- polycystic ovary syndrome
- high glucose
- protein kinase
- drug induced
- diabetic rats