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We studied the relation between the control of blood glucose and the width of skeletal-muscle capillary basement membrane in 23 insulin-dependent (Type I) diabetic patients. After initial measurement of levels of glycosylated hemoglobin and width of skeletal-muscle capillary basement membrane, the patients were divided into two groups: an experimental group of 13 patients who were treated with continuous subcutaneous insulin infusion, and a control group of 10 patients who continued to receive conventional treatment--usually two injections of insulin daily. After two years, the experimental group had a significant decrease in glycosylated hemoglobin levels as compared with base-line values (mean +/- S.E.M., 7.6 +/- 0.4 vs 10.2 +/- 0.7 per cent; P less than 0.001), reflecting improved control of blood glucose, and a significant reduction in the width of skeletal-muscle capillary basement membrane (1293 +/- 68 vs. 1717 +/- 182 A; P less than 0.05). The control group of patients had no significant change in their levels of glycosylated hemoglobin or in the width of their skeletal-muscle capillary basement membranes. If changes in the capillaries in skeletal muscle parallel those in the capillaries in retinal or renal tissue, then meticulous control of blood glucose may be beneficial over time in preventing the microvascular complications of diabetes.

Magnesium deficiency was induced in a setting of an otherwise adequate diet in adult beagle dogs. Despite the development of severe hypomagnesemia (from 1.5 +/- 0.2 to 0.5 +/- 0.2 meq/liter) during the 10-wk study, Mg content of skeletal muscle fell only modestly (from 3.8 +/- 0.2 to 3.1 +/- 0.4, P less than 0.005, at 7 wk and 3.5 +/- 0.4 mM/100 g FFDS, NS, at 10 wk). The most pronounced muscle compositional changes were a loss of phosphorus (from 29.5 +/- 1.8 to 22.0 +/- 1.6, P less than 0.001, at 7 wk and 24.8 +/- 2.8 mM/100 G FFDS, P less than 0.001, at 10 wk) and gains of calcium (from 0.64 +/- 0.11 to 0.93 +/- 0.17, P less than 0.05, at 7 wk, and 0.85 +/- 0.26 mM/100 g FFDS, P less than 0.05, at 10 wk), sodium (from 13.2 +/- 2.6 to 22.9 +/- 4.7, P less than 0.001 at 7 wk and 17.8 +/- 2.0 meq/100 g FFDS, P less than 0.005, at 10 wk), and chloride (from 5.8 +/- 0.8 to 8.2 +/- 1.6, P less than 0.001, at 7 wk and 6.8 +/- 0.6 meq/100 g FFDS, P less than 0.05, at 10 wk). Cellular potassium content did not change (from 35.9 +/- 1.9 to 33.0 +/- 4.1, NS, at 7 wk and 36.3 +/- 2.0 meq/100 g FFDS, NS, at 10 wk). Muscle cell electrical hyperpolarization developed after 10 wk of Mg depletion. Convulsive seizures developed in three animals. Frank rhabdomyolysis in three animals and focal necrosis in four animals were present on terminal biopsy, with only four animals having completely normal histology.

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Most of the Krebs cycle enzymes are believed to exist in ‘soluble’ form in the mitochondrial matrix except succinate dehydrogenase which is a part of the inner membrane (1). Citrate synthase, one of the Krebs cycle enzymes, is present in rat liver, kidney and heart mitochondria proportional to the amount of the inner membrane area rather than the matrix volume (2). Recent studies on model systems support the idea that the ‘soluble’ Krebs cycle enzymes are probably localized on the inner surface (matrix side) of the inner membrane (3-5). Localization of these enzymes in mitochondria by cytochemical or immunocytochemical methods would be crucial to determine the validity of the above hypothesis. The present study describes cytochemical localization of citrate synthase in rat heart muscle.

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