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Biomedical subjects

M Battell

Publications and source records attributed to M Battell.

5 recordsLinked to original sources
PubMed2001

Hyperinsulinemia superimposed on insulin resistance does not elevate blood pressure.

The role of hyperinsulinemia and insulin resistance in the development of hypertension is an area of much current interest. A central question that remains unanswered is whether exogenous hyperinsulinemia can elevate blood pressure (BP) in the presence of pre-existing insulin resistance. To examine this proposition, we studied the effects of chronic fructose feeding on plasma insulin levels and BP in insulin-resistant Zucker fatty rats and in lean (insulin-sensitive) controls. In addition, vascular responses to norepinephrine in aortae and mesenteric arteries were compared between groups. Zucker fatty rats were hyperinsulinemic, insulin-resistant, yet normotensive when compared with age-matched lean controls. Long term fructose feeding increased plasma insulin levels and BP in the lean group. Strikingly, the fatty rats remained refractory to fructose-induced increases in BP despite exaggeration of hyperinsulinemia. Vascular reactivity assessed in aortae and mesenteric arteries was comparable between groups. These data suggest that, in vivo, the mechanisms of hyperinsulinemia-induced hypertension are not operative in the face of pre-existing insulin resistance in obese Zucker rats.

Animals↗
PubMed1998

Kinetic analysis and comparison of uptake, distribution, and excretion of 48V-labeled compounds in rats.

Vanadium has been found to be orally active in lowering plasma glucose levels; thus it provides a potential treatment for diabetes mellitus. Bis(maltolato)oxovanadium(IV) (BMOV) is a well-characterized organovanadium compound that has been shown in preliminary studies to have a potentially useful absorption profile. Tissue distributions of BMOV compared with those of vanadyl sulfate (VS) were studied in Wistar rats by using 48V as a tracer. In this study, the compounds were administered in carrier-added forms by either oral gavage or intraperitoneal injection. Data analyzed by a compartmental model, by using simulation, analysis, and modeling (i.e., SAAM II) software, showed a pattern of increased tissue uptake with use of 48V-BMOV compared with 48VS. The highest 48V concentrations at 24 h after gavage were in bone, followed by kidney and liver. Most ingested 48V was eliminated unabsorbed by fecal excretion. On average, 48V concentrations in bone, kidney, and liver 24 h after oral administration of 48V-BMOV were two to three times higher than those of 48VS, which is consistent with the increased glucose-lowering potency of BMOV in acute glucose lowering compared with VS.

Animals↗
PubMed1995

Vanadium compounds as insulin mimics.

That vanadium compounds act in an insulin-mimetic fashion both in vitro and in vivo has been well established. Both inorganic and organic vanadium compounds have been shown to lower plasma glucose levels, increase peripheral glucose uptake, improve insulin sensitivity, decrease plasma lipid levels, and normalize liver enzyme activities in a variety of animal models of both type I and type II diabetes. Vanadium treatment of diabetic animals does not restore plasma insulin levels but may spare pancreatic insulin. Elucidation of the mechanism(s) of action and potentiation of vanadium's insulin-mimetic effect by appropriate ligand binding would seem to be the highest priorities for future investigation.

Animals↗
PubMed1994

Cardiovascular and metabolic changes in spontaneously hypertensive rats following streptozotocin administration.

OBJECTIVES: To investigate whether the high mortality rate that occurs in streptozotocin (STZ)-diabetic spontaneously hypertensive rats (SHR) is related to abnormalities in glycemic control, in hemodynamics and cardiac function, or in susceptibility to the occurrence of ventricular arrhythmias. METHODS: Diabetes was induced in SHR and Wistar-Kyoto (WKY) rats by the intravenous injection of STZ 55 mg/kg. Intraperitoneal glucose tolerance tests were performed after six and 11 weeks. Blood pressure was measured in conscious rats at weeks 0 and 11 with a tail-cuff method and in anesthetized animals at week 12 through a cannulated artery. Response of myocardial function to rapid intravenous infusion of saline 10 mL/kg/min and the times of onset of ventricular arrhythmias during intravenous infusion of aconitine 20 micrograms/kg/min were determined in anesthetized rats at week 12. Plasma samples from the rats were assayed for glucose, insulin, triglycerides and carnitine. RESULTS: STZ injection caused hyperglycemia, hypoinsulinemia and glucose intolerance equally in SHR and WKY. Diabetic SHR exhibited significant hypertriglyceridemia, depletion in plasma carnitine, impaired responses of blood pressure and myocardial function to rapid intravenous infusion of saline and a 37.5% mortality rate, whereas diabetic WKY did not exhibit these changes. SHR and WKY, diabetic or nondiabetic, were equally sensitive to the induction of ventricular arrhythmias by aconitine infusion. CONCLUSION: Mortality of the STZ-diabetic SHR is not due to an exaggeration of the impaired glycemic control, but may be attributed to the occurrence of cardiac dysfunction. The development of life-threatening cardiac arrhythmias, while unlikely, cannot be completely excluded.

Aconitine↗