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Biomedical subjects

S Chipkin

Publications and source records attributed to S Chipkin.

4 recordsLinked to original sources
PubMed2000

Glucose-insulin-potassium solutions improve outcomes in diabetics who have coronary artery operations.

BACKGROUND: This study was undertaken to determine whether glucose-insulin-potassium (GIK) would improve myocardial performance and limit morbidity after coronary artery bypass grafting in diabetic patients. METHODS: Forty consecutive coronary artery bypass grafting patients with medically treated diabetes mellitus were prospectively randomly assigned to either a GIK group (n = 20; 500 mL D5W + 80 U regular insulin + 40 mEq KCl 30 mL/hour) or a no-GIK group (n = 20; D5W at 30 mL/hour). The GIK was begun at anesthetic induction and continued for 12 hours postoperatively. RESULTS: Patients treated with GIK had higher postoperative cardiac indices (2.88 +/- 0.50 versus 2.20 +/- 0.39 L/minute per square meter; p < 0.0001), lower inotrope scores (0.40 +/- 0.68 versus 1.25 +/- 1.44; p = 0.05), less weight gain (5.80 +/- 3.76 versus 13.85 +/- 6.52 pounds; p < 0.0001), and had shorter times of ventilator support (8.35 +/- 2.60 versus 13.45 +/- 7.33 hours; p = 0.0128). They had a significantly lower prevalence of atrial fibrillation (15% versus 60%; p = 0.003), and shorter hospital stays (6.70 +/- 1.52 versus 10.15 +/- 6.62 days; p = 0.02). CONCLUSIONS: Substrate enhancement with GIK in diabetic patients improved myocardial performance and resulted in faster recovery after coronary artery bypass grafting.

Aged↗
PubMed2000

Dehydroepiandrosterone sulfate and beta-cell function: enhanced glucose-induced insulin secretion and altered gene expression in rodent pancreatic beta-cells.

Administration of dehydroepiandrosterone (DHEA), or its sulfated form (DHEAS), controls hyperglycemia in diabetic rodents without directly altering insulin sensitivity. We show that DHEAS enhanced glucose-stimulated insulin secretion when administered in vivo to rats or in vitro to beta-cell lines, without changing cellular insulin content. Insulin secretion increased from 3 days of steroid exposure in vitro, suggesting that DHEAS did not directly activate the secretory processes. DHEAS selectively increased the beta-cell mRNA expression of acyl CoA synthetase-2 and peroxisomal acyl CoA oxidase in a time-dependent manner. Although DHEAS is a peroxisomal proliferator, it did not alter the mRNA expression of peroxisomal proliferator-activated receptor (PPAR) alpha or beta, or enhance the activity of transfected PPAR alpha, beta, or gamma in vitro. Thus, DHEAS directly affected the beta-cell to enhance glucose-stimulated insulin secretion and increased the mRNA expression of specific beta-cell mitochondrial and peroxisomal lipid metabolic enzymes. This effect of DHEAS on insulin secretion may contribute to the amelioration of hyperglycemia seen in various rodent models of diabetes.

Acyl-CoA Oxidase↗
PubMed1988

The effect of small increases in dietary iodine on thyroid function in euthyroid subjects.

Dietary iodine intake in the United States is greater than that considered necessary for the maintenance of normal thyroid function. The administration of pharmacologic quantities of iodine (10 to 1,000 mg daily) to euthyroid subjects results in small decreases in the serum T4 and T3 concentrations and a compensatory increase in the basal and TRH-stimulated serum TSH concentrations. Studies were carried out to determine whether a far smaller increase in iodine intake would also affect thyroid function. Normal volunteers received 1,500, 500, or 250 micrograms supplemental iodine daily for 14 days. Following the administration of 1500 micrograms iodine daily, there were small but significant decreases in the serum T4 and T3 concentrations and a small compensatory increase in the serum TSH concentration and the serum TSH response to TRH. In contrast, no changes in pituitary-thyroid function occurred during the administration of 500 or 250 micrograms iodine daily. These findings indicate that a small increase in dietary iodine can induce subtle changes (all values remaining within the normal range) in pituitary-thyroid function, probably by inhibiting thyroid hormone release. The smaller iodine supplements of 500 and 250 micrograms daily, quantities that may easily be achieved under normal conditions, did not, however, affect thyroid function.

Adult↗