Differential proteomic and oxidative profiles unveil dysfunctional protein import to adipocyte mitochondria in obesity-associated aging and diabetes.

Human age-related diseases, including obesity and type 2 diabetes (T2DM), have long been associated to mitochondrial dysfunction; however, the role for adipose tissue mitochondria in these conditions remains unknown. We have tackled the impact of aging and T2DM on adipocyte mitochondria from obese patients by quantitating not only the corresponding abundance changes of proteins, but also the redox alterations undergone by Cys residues thereof. For that, we have resorted to a high-throughput proteomic approach based on isobaric labeling, liquid chromatography and mass spectrometry. The alterations undergone by the mitochondrial proteome revealed aging- and T2DM-specific hallmarks. Thus, while a global decrease of oxidative phosphorylation (OXPHOS) subunits was found in aging, the diabetic patients exhibited a reduction of specific OXPHOS complexes as well as an up-regulation of the anti-oxidant response. Under both conditions, evidence is shown for the first time of a link between increased thiol protein oxidation and decreased protein abundance in adipose tissue mitochondria. This association was stronger in T2DM, where OXPHOS mitochondrial- vs. nuclear-encoded protein modules were found altered, suggesting impaired mitochondrial protein translocation and complex assembly. The marked down-regulation of OXPHOS oxidized proteins and the alteration of oxidized Cys residues related to protein import through the redox-active MIA (Mitochondrial Intermembrane space Assembly) pathway support that defects in protein translocation to the mitochondria may be an important underlying mechanism for mitochondrial dysfunction in T2DM and physiological aging. The present draft of redox targets together with the quantification of protein and oxidative changes may help to better understand the role of oxidative stress in both a physiological process like aging and a pathological condition like T2DM.

Randomized prospective trial on the occurrence of laparoscopic trocar site hernias.

INTRODUCTION: Laparoscopy has become the gold standard in an increasing number of procedures. We analyze the incidence of trocar site hernias (TSH) and determine whether closure of the external fascia prevents onset of TSH and possible complications. METHODS: We performed a simple-blind randomized trial with two groups, one in which all the orifices were closed by suturing the external fascia of the abdominal wall (group A), and another in which the orifices were left open, closing only the skin (group B). Monitoring for TSH lasted 2 years from the intervention. The trial has been registered at www.clinicaltrials.gov with the clinicaltrials.gov identifier number: NCT01240434. RESULTS: A total of 195 patients were randomized. Thirty-three were removed from the study after conversion to open surgery, early open reoperation, or loss to follow-up. The remaining 162 patients comprised the study population, 80 in group A and 82 in group B. We found no differences between the groups regarding basic demographic data, kind of surgery, or topographic distribution of the trocars. Five TSH were diagnosed-four in group A and one in group B (P=.176)-and there was no relation between TSH and trocar size (11 or 12 mm) or location. We found 10 wound infections, 7 in group A and 3 in group B (P=.154). CONCLUSION: Our study suggests that the onset of TSH does not depend on trocar size or location. There is no evidence that suture of the fascial defect prevents the onset of TSH. In addition, we found a trend toward a higher incidence of wound infection among patients in whom the fascia had been sutured.