David M. Klachko

Myotonic Response Induced by Inhibitors of Cholesterol Biosynthesis

Steroid inhibitors of cholesterogenesis containing nitrogen-substituted side chains induced electromyographic myotonia in rats. Cholesterol reduction or desmosterol accumulation, per se, did not cause myotonia, and cholestrol feeding prevented drug-induced myotonia. Desmosterol accumulation in combination with a specific drug effect may cause the observed myotonia.

A Randomized, Double-Blind, Placebo-Controlled Trial to Evaluate the Effect of Enalapril in Patients With Clinical Diabetic Nephropathy

It is unknown if the antiproteinuric effect of angiotensin-converting enzyme (ACE) inhibitors reflects attenuation in the rate of progression of diabetic nephropathy. We report the results of a randomized, double-blind clinical trial designed to evaluate the longitudinal (18-month) effect of the ACE inhibitor, enalapril (5 to 40 mg/d), versus a placebo on 24-hour urinary protein excretion and on the rate of progression of renal disease in 33 patients with clinical diabetic nephropathy. Systemic blood pressure was controlled throughout the trial with conventional antihypertensive drugs. Glomerular filtration rate (GFR), determined by Tc99mDTPA renal clearance, and urinary protein excretion were monitored at 3-month intervals. Enalapril, in contrast to placebo therapy, was associated with an initial (40%) and sustained (33%) decrease in urinary protein excretion. Patients randomized to both enalapril or placebo experienced mean decreases in GFR, from 1.01 mL/s/1.73 m2 (61 mL/min/1.73 m2) to 0.85 mL/s/1.73 m2 (51 mL/min/1.73 m2), and from 1.06 mL/s/1.73 m2 (64 mL/min/1.73 m2) to 0.97 mL/s/1.73 m2 (58 mL/min/1.73 m2), respectively. Eleven of 18 patients (61%) randomized to enalapril, and 10 of 15 (66%) patients randomized to placebo, had a decrease in GFR; their rates of progression were -1.18 mL/min/1.73 m2/mo and -1.00 mL/min/1.73 m2/mo, respectively. In the absence of changes in blood pressure, the addition of an ACE inhibitor to patients with clinical diabetic nephropathy could not be shown to confer a unique renal protective effect. A prolonged decrease in 24-hour protein excretion could not be shown to predict attenuation in the progression of established clinical diabetic nephropathy.

Why people don't learn from diabetes literature: influence of text and reader characteristics

The study was designed to identify text and reader characteristics that impede learning. Twenty-six adults with diabetes mellitus took a 15-item test for prior knowledge of diabetes, a 20-item vocabulary test, and a Need for Cognition questionnaire. Immediately after reading an excerpt from a commonly used diabetes pamphlet, they could recall an average of only eight of the 108 ideas in it. Readers seldom monitored their comprehension. Also, the topics that they thought were important differed from the topics that a physician thought were important. Many readers lacked reading skills, but those with high need for cognition and higher vocabulary scores recalled more topics. Even with an appropriate reading level, text characteristics that could hinder comprehension included lack of organization and clarity.

Hypersensitivity of diabetic human platelets to platelet activating factor

Platelet activating factor (PAF) stimulated aggregation and [32P]-phosphatidic acid (PA) production was compared in normal and diabetic human subjects in platelet rich plasma. The concentration of PAF for half maximal (50%) aggregation of normal and diabetic platelets was 50 nM and 8 nM, respectively. PAF stimulated [32P]-PA production (a metabolite of phospholipase C pathway) was also greater in the platelets from diabetic subjects. This [32P]-PA production was inhibited by the PAF receptor antagonists SRI-63441 and SRI-63675. When the levels of glycosylated hemoglobin (HbA1c) were compared with the PAF stimulated [32P]-PA production a significant relationship was observed. These studies have demonstrated for the first time that diabetic human platelets show hypersensitivity to PAF in both aggregation and [32P]-PA production compared to normal subjects. This may be a result of some modification in phospholipid turnover mechanism and is receptor mediated. Further, the relationship of the degree of aggregation and [32P]-PA production to the level of HbA1c suggest that the insulin deficiency may contribute to these effects.

The endocrine pancreas and juvenile diabetes

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Regulation of intermediary metabolism by nucleotides: The mechanism of action of insulin

Abstract Certain pathways of biosynthesis require the provision of energy by specific nucleoside triphosphates (e.g. uridine triphosphate for glycogen synthesis, guanosine triphosphate for protein synthesis, and cytidine triphosphate for synthesis of phospholipids), and the rate of synthesis may be controlled by the amount of the specific nucleoside triphosphate available at the time. It is postulated that certain peptide hormones act on the nucleotide transphosphorylases and, by regulating the relative quantities of nucleoside triphosphates in the cell, indirectly control intermediary metabolism. Insulin appears to act by accelerating the transfer of high energy phosphate from ATP to all the non-adenosine nucleoside diphosphates, thus causing a general increase in rate of synthesis and storage in the cell. A possible single site for this action is on the enzyme, nucleoside diphosphokinase.

Discussion Following Talks on Microvascular Complications of Diabetes Mellitus

To open this discussion period, we have asked Dr. John Town-send, who is in the Department of Pathology here at the University of Missouri, to make a few comments regarding the colony of genetically diabetic animals that they have been following here in regard to vascular disease in these animals.