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Daligcon, B. C.

Publications and source records attributed to Daligcon, B. C..

5 records
All sourcesNASA NTRSDOE OSTI
NASA NTRS1985

Hyper-G stress-induced hyperglycemia in rats mediated by glucoregulatory hormones

The present investigation is concerned with possible relations of the hyperglycemic response of rats exposed to hyper-G stress to (1) alterations in blood levels of the glucoregulatory hormones and gluconeogenic substrates, and (2) changes in insulin response on muscle glucose uptake. Male Sprague-Dawley rats weighing 250-300 g were used in the study. The results of the experiments indicate that the initial rapid rise in blood glucose of rats exposed to hyper-G stress is mediated by increases in circulating catecholamines and glucagon, both potent stimulators of hepatic gluconeogenesis. Lactate, derived from epinephrine stimulation of muscle glycogenolysis, appears to be a major precursor for the initial rise in blood glucose. The inhibition of the insulin-stimulated glucose uptake by muscle tissues may be a factor in the observed sustained hyperglycemia.

Daligcon, B. C.↗
NASA NTRS1985

Increased gluconeogenesis in rats exposed to hyper-G stress

The effect of glucogenesis on the plasma glucose and liver glycogen of rats exposed to hyper-G stress is investigated. Twelve male Sprague-Dawley rats are injected with C-14 lactate, alanine, of glycerol, and six of the rats are exposed to 3.1 G for 0.25, 0.50, and 1.0 hr. The plasma glucose and liver glycogen of the centrifuged and noncentrifuged rats are analyzed. A significant increase in the C-14 incorporation of the substrate into the plasma glucose and liver glycogen is observed in the centrifuged rats. The injection of 5-methoxyindole-2-carboxylic acid, a gluconeogenesis inhibitor, results in a blocked increase in plasma glucose and liver glycogen. The role of epinephrine on the hyperglycemic and liver glycogen responses of centrifuged rats is studied. It is concluded that the initial increase in plasma glucose and liver glycogen in rats exposed to hyper-G stress is the result of an increased rate of gluconeogenesis.

Daligcon, B. C.↗
NASA NTRS1985

Increased gluconeogenesis in rats exposed to hyper-G stress

The effect of gluconeogenesis on the levels of plasma glucose and liver glycogen was studied in rats exposed to hyper-G stress. Incorporation of lactate, alanine, or glycerol, labeled with C-14, into plasma glucose and liver glycogen was measured in rats centrifuged at 3.1 G for 0.25, 0.50, and 1.0-hr periods, and was compared to noncentrifuged controls injected with appropriate glycogen precursors. It was found that exposure to G-stress leads to increased incorporation from all three substrates into both plasma glucose and liver glycogen. These early incorporation increases were blocked upon pre-G administration of 5-methoxyindole-2-carboxylic acid, a gluconeogenesis inhibitor, or propanolol, a beta-adrenergic blocker, as well as by adrenodemedullation. Results indicate that the rapid rise in plasma glucose, as well as in liver glycogen in rats exposed to hyper-G stress is due to an increased rate of gluconeogenesis, and that epinephrine, released in response to hyper-G-induced activation of the sympathetic-adrenal system, plays a dominant role during the early stages of hyper-G stress.

Daligcon, B. C.↗
NASA NTRS1982

Increased gluconeogenesis in hyper-G stressed rats

The role of gluconeogenesis in the altered carbohydrate metabolism in rats exposed to hyper-G stress is investigated. The blood levels of the substrates and hormones involved in gluconeogenesis were determined in rats exposed to 3.1 G for various time periods (0.25 to 24 hr). It is found that hyper-G stressed rats showed an immediate increase in plasma glucose at the onset of centrifugation which persisted throughout all the exposure periods. A substantial part of the initial rise in blood glucose is attributed to an increased rate of gluconeogenesis. An increase in liver glycogen deposition was observed in centrifuged rats as early as 0.50 hr exposure time, with progressively larger amounts accumulated as the exposure time was extended to 24 hr. It is concluded that the increase in gluconeogenic activity of hyper-G stressed rats is due to an increase in the mobilization of gluconeogenic substrates from perpheral tissues to the liver as a result of increases in circulating catecholamines and glucagon.

Daligcon, B. C.↗