Impaired Mitochondrial Function and Insulin Resistance of Skeletal Muscle in Mitochondrial Diabetes  

Oleh:

Szendroedi, Julia ; Schmid, Albrecht Ingo ; Meyerspeer, Martin ; Cervin, Camilla ; Kacerovsky, Michaela

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Diabetes Care vol. 32 no. 04 (Apr. 2009), page 677-679 .

Ketersediaan

Perpustakaan FK Nomor Panggil: D05.K.2009.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

OBJECTIVE Impaired muscular mitochondrial function is related to common insulin resistance in type 2 diabetes. Mitochondrial diseases frequently lead to diabetes, which is mostly attributed to defective ß-cell mitochondria and secretion. RESEARCH DESIGN AND METHODS We assessed muscular mitochondrial function and lipid deposition in liver (hepatocellular lipids [HCLs]) and muscle (intramyocellular lipids [IMCLs]) using 31P/1H magnetic resonance spectroscopy and insulin sensitivity and endogenous glucose production (EGP) using hyperinsulinemic-euglycemic clamps combined with isotopic tracer dilution in one female patient suffering from MELAS (myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) syndrome and in six control subjects. RESULTS The MELAS patient showed impaired insulin sensitivity (4.3 vs. 8.6 ± 0.5 mg · kg-1 · min-1) and suppression of EGP (69 vs. 94 ± 1%), and her baseline and insulin-stimulated ATP synthesis were reduced (7.3 and 8.9 vs. 10.6 ± 1.0 and 12.8 ± 1.3 µmol · l-1 · min-1) compared with those of the control subjects. HCLs and IMCLs were comparable between the MELAS patient and control subjects. CONCLUSIONS Impairment of muscle mitochondrial fitness promotes insulin resistance and could thereby contribute to the development of diabetes in some patients with the MELAS syndrome.

Opini Anda

Klik untuk menuliskan opini Anda tentang koleksi ini!

Kembali