Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.3.5.1 (succinate dehydrogenase)
 8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phagocytic vesicles were obtained by density gradient centrifugation of homogenized rabbit alveolar macrophages that had ingested emulsified paraffin oil contained Oil Red O. The phagocyte vesicles floated and thereby were separated from the soluble fraction and from other cell components which sedimented. The purity of the isolated vesicles was documented by electron microscopy, chemical and enzyme analysis. The vesicles contained 87% of the cell-associated Oil Red O, and were essentially free of DNA, RNA, succinic dehydrogenase, and glucose-6-phosphatase. Acid phosphatase, beta-glucuronidase, and catalase were transferred from the sedimenting fraction to the phagocytic vesicle fraction during phagocytosis, whereas enzyme activities of the soluble fraction remained unchanged. Half of the catalase of resting macrophages was in the pellet fraction and, compared with acid phosphatase, greater amounts of digitonin were required to release full activity. Such differential latency has been described for enzymes of peroxisomes vs. those of lysosomes. Compared with polymorphonuclear leukocyte vesicles studied previously, phagocytic vesicles of macrophages had more electron-dense material and lower Oil Red O:protein, phospholipid:protein, and enzyme:protein ratios. It is thus probable that secondary lysosomes become part of the macrophage vesicle. When paraffin oil particles, the stimulus for phagocytic vesicle formation, were washed away from the macrophages, acquisition of hydrolases by preformed vesicles ceased, i.e. transfer of these enzymes into phagocytic vesicles occurred only during or shortly after the formation of new vesicles. As noted previously by others, the content of acid hydrolases of stimulated alveolar macrophages was doubled in comparison to normal cells. The difference between stimulated and normal macrophages was even more marked when isolated phagocytic vesicles were analyzed. Vesicles from stimulated macrophages had 3-5 times more enzyme activity (per milligram of vesicle protein or per amount of paraffin oil ingested) than did vesicles from normal cells.
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PMID:Isolation and properties of phagocytic vesicles. II. Alveolar macrophages. 501 Nov 3

We examined the hypothesis that an excess accumulation of intramuscular lipid (IMCL) is associated with insulin resistance and that this may be mediated by the oxidative capacity of muscle. Nine sedentary lean (L) and 11 obese (O) subjects, 8 obese subjects with type 2 diabetes mellitus (D), and 9 lean, exercise-trained (T) subjects volunteered for this study. Insulin sensitivity (M) determined during a hyperinsulinemic (40 mU x m(-2)min(-1)) euglycemic clamp was greater (P < 0.01) in L and T, compared with O and D (9.45 +/- 0.59 and 10.26 +/- 0.78 vs. 5.51 +/- 0.61 and 1.15 +/- 0.83 mg x min(-1)kg fat free mass(-1), respectively). IMCL in percutaneous vastus lateralis biopsy specimens by quantitative image analysis of Oil Red O staining was approximately 2-fold higher in D than in L (3.04 +/- 0.39 vs. 1.40 +/- 0.28% area as lipid; P < 0.01). IMCL was also higher in T (2.36 +/- 0.37), compared with L (P < 0.01). The oxidative capacity of muscle determined with succinate dehydrogenase staining of muscle fibers was higher in T, compared with L, O, and D (50.0 +/- 4.4, 36.1 +/- 4.4, 29.7 +/- 3.8, and 33.4 +/- 4.7 optical density units, respectively; P < 0.01). IMCL was negatively associated with M (r = -0.57, P < 0.05) when endurance-trained subjects were excluded from the analysis, and this association was independent of body mass index. However, the relationship between IMCL and M was not significant when trained individuals were included. There was a positive association between the oxidative capacity and M among nondiabetics (r = 0.37, P < 0.05). In summary, skeletal muscle of trained endurance athletes is markedly insulin sensitive and has a high oxidative capacity, despite having an elevated lipid content. In conclusion, the capacity for lipid oxidation may be an important mediator of the association between excess muscle lipid accumulation and insulin resistance.
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PMID:Skeletal muscle lipid content and insulin resistance: evidence for a paradox in endurance-trained athletes. 1173 35

We previously reported an "athlete's paradox" in which endurance-trained athletes, who possess a high oxidative capacity and enhanced insulin sensitivity, also have higher intramyocellular lipid (IMCL) content. The purpose of this study was to determine whether moderate exercise training would increase IMCL, oxidative capacity of muscle, and insulin sensitivity in previously sedentary overweight to obese, insulin-resistant, older subjects. Twenty-five older (66.4 +/- 0.8 yr) obese (BMI = 30.3 +/- 0.7 kg/m2) men (n = 9) and women (n = 16) completed a 16-wk moderate but progressive exercise training program. Body weight and fat mass modestly but significantly (P < 0.01) decreased. Insulin sensitivity, measured using the euglycemic hyperinsulinemic clamp, was increased (21%, P = 0.02), with modest improvements (7%, P = 0.04) in aerobic fitness (Vo2peak). Histochemical analyses of IMCL (Oil Red O staining), oxidative capacity [succinate dehydrogenase activity (SDH)], glycogen content, capillary density, and fiber type were performed on skeletal muscle biopsies. Exercise training increased IMCL by 21%. In contrast, diacylglycerol and ceramide, measured by mass spectroscopy, were decreased (n = 13; -29% and -24%, respectively, P < 0.05) with exercise training. SDH (19%), glycogen content (15%), capillary density (7%), and the percentage of type I slow oxidative fibers (from 50.8 to 55.7%), all P < or = 0.05, were increased after exercise. In summary, these results extend the athlete's paradox by demonstrating that chronic exercise in overweight to obese older adults improves insulin sensitivity in conjunction with favorable alterations in lipid partitioning and an enhanced oxidative capacity within muscle. Therefore, several key deleterious effects of aging and/or obesity on the metabolic profile of skeletal muscle can be reversed with only moderate increases in physical activity.
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PMID:Exercise-induced alterations in intramyocellular lipids and insulin resistance: the athlete's paradox revisited. 1831 52

This was a study of the microscopic, ultrastructural, immunohistochemical, and enzyme cytochemical features of giant eosinophilic granules encountered in pancreatic acinar cells of alloxan-induced diabetic rats. Seven male F344 rats with diabetes induced by a single i.v. dose of alloxan were sacrificed after twenty-five weeks of treatment. Histologically, the pancreatic acini were diffusely atrophied, and the islets showed marked atrophy or had disappeared, and giant eosinophilic granules and small vacuoles were observed in almost all acinar cells. The eosinophilic granules showed negative reactions for periodic acid-Schiff (PAS) and acid phosphatase, as well as fat stains such as Nile blue, Oil red O, and Sudan III. Ultrastructurally, the giant eosinophilic granules were huge structures surrounded by a double membrane containing many irregular cristae. A large amount of small lipid droplets was also apparent in the basal area of the acinar cells. Immunohistochemical analysis of prohibitin, a kind of protein located in the mitochondrial inner membrane, was partially positive in the marginal area of some giant eosinophilic granules, but negative for the central area. The enzyme activity for succinic dehydrogenase (SDH), one of the mitochondrial enzymes, showed a localizing pattern similar to that of prohibitin. These findings confirmed that the giant eosinophilic granules in the exocrine pancreas of alloxan-induced diabetic rats were giant mitochondria.
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PMID:Giant mitochondria in pancreatic acinar cells of alloxan-induced diabetic rats. 2044 86