sodium-bicarbonate and Hyperinsulinism

Calcium channel blockers (CCBs) are some of the most commonly used medications in clinical practice to treat hypertension, angina, cardiac arrhythmias, and some cases of heart failure. Recent data show that CCBs are the most common of the cardiovascular medications noted in intentional or unintentional overdoses.(1) Novel treatment approaches in the form of glucagon, high-dose insulin therapy, and intravenous lipid emulsion therapies have been tried and have been successful. However, the evidence for these are limited to case reports and case series. We take this opportunity to review the various treatment options in the management of CCB overdoses with a special focus on high-dose insulin therapy as the emerging choice for initial therapy in severe overdoses.

Topics: Airway Management; Calcium Channel Blockers; Calcium Compounds; Catecholamines; Drug Overdose; Fat Emulsions, Intravenous; Glucagon; Humans; Hyperinsulinism; Sodium Bicarbonate

Insulin autoimmune syndrome is a rare cause of hyperinsulinemic hypoglycemia characterized by autoantibodies to human insulin without previous insulin use. We report a case of a patient with hyperinsulinemic hypoglycemia possibly caused by insulin antibodies induced by insulin analogs and a novel therapeutic measure for this condition.. An 84-year-old Japanese man with a 28-year history of type 2 diabetes and chronic kidney disease, treated with biphasic insulin aspart 30, experienced persistent early morning hypoglycemia with daytime hyperglycemia. Despite discontinuation of biphasic insulin aspart 30, the condition persisted even after the patient ate small, frequent meals. Sodium bicarbonate was administered to correct the chronic metabolic acidosis, which then rectified the early morning glucose level.. We believe this to be the first published case of a therapeutic approach to the treatment of hyperinsulinemic hypoglycemia associated with insulin antibodies that factors in blood pH and the correction of acidosis using sodium bicarbonate, which physicians could consider.

Topics: Acidosis; Aged, 80 and over; Alkalies; Autoimmune Diseases; Humans; Hyperinsulinism; Hypoglycemia; Insulin Antibodies; Male; Sodium Bicarbonate; Syndrome

Data documenting the isolated effect of systemic hyperinsulinemia on whole body and skeletal muscle leucine carbon kinetics in humans are limited. Using steady-state [14C]leucine kinetics, 10 normal volunteers were studied in the baseline postabsorptive state and then under euglycemic, hyperinsulinemic (71 +/- 5 microU/ml), and euleucinemic conditions. Systemic hyperinsulinemia resulted in a significant decrease in whole body and forearm leucine rate of appearance (Ra) by 17 and 37%, respectively, (P less than 0.0003, 0.03), without a significant change in the nonoxidized rate of disappearance for either (P = 0.23, 0.66). The baseline contribution of total body skeletal muscle (TBSM) leucine Ra and rate of disappearance (Rd) to whole body leucine Ra and Rd was 27 +/- 6 and 24 +/- 5%, respectively. During hyperinsulinemia TBSM Ra decreased by 34%, whereas whole body Ra decreased by 16%. We conclude that the primary effect of insulin in the whole body and skeletal muscle is to decrease leucine release from protein without a significant effect on leucine incorporation into protein. This antiproteolytic effect of insulin is more pronounced in skeletal muscle than in other tissues in the body.

Topics: Amino Acids; Bicarbonates; Carbon Radioisotopes; Female; Humans; Hyperinsulinism; Insulin; Kinetics; Leucine; Male; Middle Aged; Models, Biological; Muscles; Radioisotope Dilution Technique; Sodium; Sodium Bicarbonate

The effect of insulin on leg and whole body protein turnover was determined by leg exchange and plasma kinetics of [15N]phenylalanine and [1-13C]leucine during amino acid (AA) sufficiency. Eight healthy subjects were studied during AA infusion alone and during infusion of glucose and insulin (0.29 nmol.m-2.min-1) with additional AA. Insulin strongly stimulated the positive leg AA balance seen with AA (AA alone, 2.6 +/- 6.1 vs. insulin + AA, 33.1 +/- 5.8 nmol phenylalanine . 100 g leg-1.min-1; P less than 0.001). Phenylalanine uptake by leg tissues rose during insulin plus AA (47.3 +/- 11.5 vs. 73.1 +/- 7.3 nmol. 100 g-1.min-1; P = 0.022) but with only a slight reduction in leg phenylalanine release (44.7 +/- 8.1 vs. 40.0 +/- 7.9 nmol.100 g-1.min-1). Leg nonoxidative leucine plus alpha-ketoisocaproate (KIC) uptake was increased slightly with insulin (129 +/- 26 vs. 146 +/- 21 nmol.100 g-1. min-1), but leg leucine oxidation increased fourfold (P = 0.012). Leg leucine plus KIC release was reduced by insulin (120 +/- 17 vs. 84 +/- 10 nmol.100 g-1.min-1; P = 0.005); endogenous leucine appearance of leucine and phenylalanine decreased with insulin (leucine, 1.97 +/- 0.08 vs. 1.65 +/- 0.10; phenylalanine, 0.76 +/- 0.03 vs. 0.54 +/- 0.08 mumols.kg-1.min-1; P less than 0.02). The results suggest that insulin, given with sufficient amino acids, may stimulate leg and whole body protein balance by mechanisms including stimulation of protein synthesis and inhibition of protein breakdown.

Topics: Adult; Amino Acids; Bicarbonates; Carbon Isotopes; Female; Glucose; Glucose Clamp Technique; Humans; Hyperinsulinism; Insulin; Kinetics; Leucine; Male; Muscles; Nitrogen Isotopes; Phenylalanine; Sodium; Sodium Bicarbonate