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Biomedical subjects

J E Aiyathurai

Publications and source records attributed to J E Aiyathurai.

At least 19 recordsLinked to original sources
PubMed1991

Regulation of glucose uptake by stressed cells.

Lactate production by BHK cells is stimulated by arsenite, azide, or by infection with Semliki Forest virus (SFV). In the case of arsenite or SFV infection, the increase correlates approximately with the increase in glucose transport as measured by uptake of [3H] deoxy glucose (dGlc); in the case of azide, the increase in lactate production exceeds that of glucose transport. Hence glucose utilization by BHK cells and its stimulation by anaerobic and other types of cellular stress is controlled at least in part at the level of glucose transport. The glucose uptake by BHK cells is also stimulated by serum and by glucose deprivation. In these circumstances, as with arsenite, stimulation is reversible, with t1/2 of 1-2 hours; stimulation is compatible with a translocation of the glucose transporter protein between an intracellular site and the plasma membrane (shown here for serum and previously for arsenite). The surface binding and rate of internalization of [125I]-labelled transferrin and [125I] alpha 2-macroglobulin was studied to determine whether changes in glucose transport are accompanied by changes in the surface concentration or rate of internalization of membrane proteins. The findings indicate that changes in glucose transport do not reflect a consistent and general redistribution of membrane receptors. Taken together, the results are compatible with the proposal that BHK cells exposed to stimuli like insulin or serum, or to stresses like arsenite, azide, SFV infection, or deprivation of glucose, respond in the same manner: namely, by an increased capacity to transport glucose brought about by reversible and specific translocation of the transporter protein from an (inactive) intracellular site to the plasma membrane.

Anaerobiosis↗
PubMed1986

Lactate production in type B hyperlactataemia due to infective encephalopathy.

We have suggested that the neuroglycopenia of infective encephalopathy results in increased lactate production in muscle as an alternative cerebral fuel. Two probable mechanisms for enhanced lactate production in infective encephalopathy are fatty acidaemia and increased LDH activity. Hyperglycaemia-producing infusions should then result in clinical and metabolic recovery. Twenty-two children with encepahlopathy were studied over 2 1/2 week periods. There was normoglycaemia at admission together with hyperlactataemia (p less than 0.004), fatty acidaemia (p less than 0.004) and increased serum LDH activity (p less than 0.005). Therapeutic hyperglycaemia resulted in recovery and a progressive return of metabolic aberrations to normality. Two case reports detail the responses to such management.

Blood Glucose↗
PubMed1983

Role of glucose homeostatic mechanisms in viral infections.

Though normoglycaemia is thought to indicate adequacy of cellular glucose content, ketoacidosis occurs in viral infections even in the presence of normo- and hyperglycaemia. These wide variations in glucose concentrations may reflect the patients' adaptive abilities in situations where glucose transport is impaired by viruses. Hypoglycaemia would suggest poor adaptation and hyperglycaemia good adaptation. Increased free fatty acid (FFA) concentrations and enzyme activity are probable adaptive mechanisms. If so, they should decrease with hyperglycaemia-producing infusions. Profiles of glucose, FFA, enzymes, and fever over 19 days in 24 children with viral infections are reported. On admission 87.5% were normo- or hyperglycaemic with increased FFA, AST, LDH, and fever (P less than 0.005) when compared with values 19 days later. With infusions that produced hyperglycaemia, there was clinical recovery with a decrease in FFA and enzyme activity. The hyperglycaemia observed in 56.5% therefore points to glucose homeostatic mechanisms being geared to maintain the intracellular milieu. Hence normoglycaemia does not always indicate cellular glucose adequacy.

Acute Disease↗
PubMed1983

The significance of type B hyperlactataemia in infective encephalopathy.

A disordered sensorium, a cardinal sign of lactic acidosis, is commonly attributed to the acidosis resulting from increased production and decreased utilization of lactate. We report hyperlactataemia in 22 children with encephalopathy following viral, rickettsial and bacterial infections. On admission there was normoglycaemia together with anion gap acidosis (p less than 0.02), hyperlactataemia (p less than 0.003), fatty acidaemia (p less than 0.004) and increased serum creatinine (p less than 0.0004) when compared to the results in convalescence. Management with two types of hyperglycaemia-producing infusions, one of them containing lactate, resulted in hyperglycaemia (p less than 0.002) from the 2nd to 4th days of admission. This was associated with a decrease in lactate, creatinine and acidosis and with clinical recovery. Infusions of either glucose or lactate would normally result in hyperlactataemia, more so if there was difficulty with lactate utilization. The fall in lactate supports the hypothesis that the hyperlactataemia is probably due to an adaptive increase in lactate production as an alternative cerebral fuel which is consequent on poor glucose utilization by brain, the cause of the encephalopathy. Additionally it leads to increased Cori cycle activity. Hence the clinical and metabolic recovery with such management.

Acidosis↗