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Objective: Obesity is an independent risk factor for chronic kidney disease. Recently, urinary mitochondrial DNA (mtDNA) has been used as a surrogate marker of mitochondrial damage in various kidney diseases. However, there are no data regarding its use in patients with obesity or the change in urinary mtDNA copy number after surgery., Design: We prospectively recruited age- and sex-matched healthy volunteers and patients with obesity (n = 22 in each group: nine men and 13 women). The copy number of urinary and serum mtDNA nicotinamide adenine dinucleotide dehydrogenase subunit-1 (mtND-1) and cytochrome-c oxidase 3 (mtCOX-3) was measured using quantitative PCR. We measured urinary mtDNA and body weight and carried out laboratory tests, 6 months after surgery., Results: Urinary mtND-1 copy number was significantly higher in the obese group than in healthy volunteers. However, urinary mtCOX-3 and serum ND-1 copy numbers in the obese group did not differ from that in the healthy volunteers. When patients with obesity were divided into two groups, according to their baseline mtND-1 copy number, bariatric surgery reduced the mtND-1 copy number (P = 0.006) in the high baseline mtDNA copy-number group. The change in urinary mtND-1 copy number was correlated with a change in urinary albumin (r = 0.478, P = 0.025)., Conclusions: Obesity is associated with elevated urinary mtND-1 copy number. Bariatric surgery reduces the elevated urinary mtND-1 copy number in patients with obesity. This suggests that bariatric surgery could attenuate mitochondrial damage in the kidney cells of patients with obesity., (Copyright © 2019 Endocrine Society.)

Diabetes mellitus is associated with increased ROS generation, oxidative injury and obesity. To elucidate the relationship between nutrition and ROS generation, we have investigated the effect of glucose challenge on ROS generation by leucocytes, p47phox protein, a key protein in the enzyme NADPH oxidase and alpha-tocopherol levels. Blood samples were drawn from 14 normal subjects prior to, at 1, 2 and 3 h following ingestion of 75 g glucose. ROS generation by polymorphonuclear leucocytes (PMNL) and mononuclear cells (MNC) increased to a peak of 244 +/- 42% and 233 +/- 34% of the basal respectively at 2h. The levels of p47phox in MNC homogenates increased significantly at 2 h and 3 h after glucose intake. alpha-Tocopherol levels decreased significantly at 1 h, 2 h and 3 h. We conclude that glucose intake stimulates ROS generation and p417phox of NADPH oxidase; increases oxidative load and causes a fall in alpha-tocopherol concentration.

Respiratory chain enzyme activities were studied in lymphocytes from patients with Parkinson disease (PD) (n = 16) and age-matched control subjects (n = 15). The patients had received no therapy before the study was conducted. Complex I, III, and IV activities were significantly lower (P < 0.05) in patients than in control subjects. A complex I defect was found in one patient, whereas complex IV was defective in another. Two patients had combined defects of both complexes. The use of lymphocytes for investigating the respiratory chain enzymes provides an easy, noninvasive method to assess mitochondrial function in patients with PD. Furthermore, our study supports the hypothesis that a biochemical defect in the respiratory chain may be involved in the pathogenesis of PD.