Search PubMed⌕ Search

Biomedical subjects

R Assan

Publications and source records attributed to R Assan.

At least 127 records · Page 7Linked to original sources
PubMed1981

Changes in circulating fuels, pancreatic hormones and liver glycogen concentration in fasting or suckling newborn pigs.

The effect of fasting or suckling on blood glucose, circulating fuels, pancreatic hormones and liver glycogen concentration have been measured in newborn pigs during the first 48 h of life. Blood glucose concentrations fell to hypoglycaemic values after 48 h of fasting whereas for the same period of time, suckling piglets maintain a normal blood glucose. These differences are not due to hepatic glycogen mobilization, since liver is totally depleted from its high glycogen stores 24 h after birth, both in fasting and suckling piglets. Blood lactate is present at a high concentration during the first 48 h, both in fasting and suckling piglets. In contrast, blood pyruvate concentration is lower in suckling than in fasting newborn pigs. Colostrum intake leads to an increase in blood amino acid concentrations in the suckling piglets in comparison with the fasting newborn. Plasma non-esterified fatty acid levels and blood glycerol concentrations are lower in fasting piglets than in the suckling ones. In suckling newborn pigs, circulating ketone bodies are very low despite the increase in non-esterified fatty acids levels. The decrease in plasma insulin/glucagon molar ratio at birth, is due to a decrease in plasma insulin and an increase in plasma glucagon, both in fasting and suckling piglets. Plasma insulin and glucagon concentrations are higher during suckling than during fasting. The data suggest that gluconeogenesis could be impaired, in fasting newborn pigs, by a low plasma glucagon level and/or a limiting availability of non-esterified fatty acids.

Amino Acids↗
PubMed1980

Carnitine improves lipid anomalies in haemodialysis patients.

51 chronic haemodialysis patients with hypertriglyceridaemia were given a daily oral dose of 2.4 g D,L-carnitine for 30 days to investigate a possible hypolipaemic effect. After 30 days' D,L-carnitine treatment the mean (+/- SEM) serum triglyceride concentration had decreased significantly from 3.50 +/- 0.39 to 2.87 +/- 0.27 mmol/l. Serum total cholesterol did not change. However, HDL cholesterol increased significantly from 0.89 +/- 0.05 to 1.35 +/- 0.07 mmol/l. This decrease in serum triglycerides and return of HDL cholesterol to normal levels in haemodialysis patients may be the result of correction of carnitine deficiency. Such treatment could reduce the risk factors for atherosclerosis and coronary-artery disease in uraemic patients.

Adult↗
PubMed1980

Fetal metabolic response to phloridzin-induced hypoglycemia in pregnant rats.

Phloridzin, an inhibitor of renal sugar transport, produces an important loss of glucose in urine of treated animals. In order to reduce severely the maternal glucose supply to the fetuses in short-term experiments, we have combined phloridzin administration to pregnant rats with 18 h starvation. Fetuses from starved phloridzin-treated mothers were compared with fetuses from starved mothers. Combined treatment markedly decreases fetal blood glucose concentration (-36%) and fetal liver glycogen stores (-76%). These changes are associated with a decrease in plasma insulin (-25%), a rise in plasma glucagon (+120%) and a marked increase of hepatic PEPCK activity (+400%). It appears from these results that phloridzin treatment for a short duration is able to induce glycogenolysis and the premature appearance of PEPCK in the liver of rat fetuses.

Animals↗
PubMed1980

Glucagon release induced by ventrolateral hypothalamic stimulation in the rat.

Catheterization of the portal vein and stereotaxic implantation of electrodes in the ventrolateral hypothalamus (VLH) were performed in normal rats after thiopental anesthesia. Immunoreactive glucagon (IRG), insulin (IRI), And glucose were monitored in portal plasma before and during electrical stimulation of the VLH (6 micro A, 50 Hz, 2 msec each, for 15 min). This stimulation induced a significant and reproducible IRG rise, followed by hyperglycemia. IRI remained unchanged. These alterations were not observed in control rats, i.e. in the absence of implantation; after VLH implantation without stimulation; or after implantation in the hippocampus or in the nucleus lenticularis. Bilateral splanchnicectomy abolished the IRG rise and hyperglycemia which followed VLH stimulation, while IRI was elevated both before and during electrical stimulation. Bilateral vagotomy did not suppress the A cell response to VLH stimulation, and it significantly reduced the IRI concentration in both basal and stimulatory periods. This resulted in sustained hyperglycemia. Attempts at total denervation of the pancreas induced patterns similar to that observed after splanchnicectomy alone. These results suggest that stimulation of the VLH can influence the endocrine pancreas and blood glucose levels by sympathetic nervous inputs which stimulate A cells and inhibit B cells.

Animals↗
PubMed1979

[The effects of acebutolol on endocrine and metabolic reactions induced by acute hypoglycaemia. Study in normal subjects and in insulin-dependent diabetics (author's transl)].

Six normal subjects and six normotensive insulin-dependent diabetics underwent two insulin hypoglycaemia tests after administration for three days of either a placebo or of acebutolol--a cardioselective beta-blocker--at a dose of 400 mg per day. The order in which the tests were performed was decided by random selection. Acebutolol suppressed the tachycardia which occurred as a reaction to hypoglycaemia but did not interfere with other warning symptoms and signs. In both normal subjects and diabetics, acebutolol neither worsened the initial hypoglycaemia nor did it delay a return to normal values. The increase in lactate levels following hypoglycaemia was not reduced by acebutolol but free fatty acid rebound was suppressed. Hormonal responses (glucagon, cortisol, growth hormone) were unaffected by the beta-blocker. If they are confirmed by long term studies, these results would suggest that acebutolol is safer to use than non-cardioselective beta-blockers in the treatment of coronary insufficiency and of hypertension in diabetics exposed to the risk of hypoglycaemia.

Acebutolol↗
PubMed1979

Glucagon and diabetes mellitus.

The present status of knowledge about glucagon pathophysiology in diabetes is reviewed. 1) A-cells behave abnormally in all varieties of diabetes mellitus, spontaneous and experimental, except perhaps in case of pancreatectomized humans. These abnormalities are : hyperreactivity of A-cells to arginine, non suppressibility by glucose, and absence of stimulation following hypoglycemia. 2) These abnormalities appear as secondary in most instances : a) A-cells behave in a normal way in most studies with prediabetics ; b) plasma glucagon concentration is normalized by excellent control of diabetes or following prolonged insulin infusion. High doses of insulin are required most of the times to obtain a normalization of A-cell function : in insulin-dependent diabetics, the physiological portoperipheral insulin gradient no longer exists, and the high doses of insulin which are necessary may be the only mean to reconstitute the high insulin concentrations supposed to be present at the A-cell level. 3) Conflicting results have been collected about the role of this glucagon excess in aggravating the diabetic metabolic syndrome. Evanescent effects follow sustained glucagon infusions: but in diabetics, glucagon bursts rather than permanent hyperglucagonemia are observed and these appear deleterious to glucose tolerance. It seems clear however that insulin deprivation is required for the full expression of the consequences of glucagon excess.

Animals↗