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Biomedical subjects

R Assan

Publications and source records attributed to R Assan.

At least 163 records · Page 9Linked to original sources
PubMed1977

Fetal metabolic response to maternal fasting in the rat.

To determine the fetal response to altered maternal fuel supply, the effects of prolonged maternal fasting, begun 24-96 h before term, were examined and compared with values from normally fed term animals. Fetal weight decreased only after 48 h of maternal fasting. Prolonged maternal fasting was associated with low blood glucose, high blood ketone bodies, and decreased gluconeogenic substrate in the fetus. Plasma insulin was decreased, whereas plasma glucagon was increased in the fetus of fasted mothers. Infusion of [2-3H]glucose into the mother to constant specific activity gave a ratio of maternal to fetal glucose activity of 1.0 in fed and 1.56 in fasted mothers. Fetal liver from fasted mothers showed both increase in activity of key gluconeogenic enzymes (glucose-6-phosphatase and phosphoenolpyruvate carboxykinase) and increased conversion in vitro of lactate, alanine, serine, and glycerol in glucose by liver slices. It is inferred that maternal fasting induces fetal substrate alterations and hormonal changes appropriate to premature appearance of hepatic gluconeogenesis. The priority for endogenous fuel provision in this state leads to impaired fetal growth.

Amino Acids↗
PubMed1977

Glucagon secretion induced by natural and artificial amino acids in the perfused rat pancreas.

The glucagon-secreting potency of 22 amino acids was investigated in the rat isolated perfused pancreas. Arginine and the structurally related amino acids were the most potent A2-cell stimulators that induced a biphasic and sustained glucagon release. Dose-response curver were different for L(+) and D(+)arginine, and the suppressor effect of glucose on the response to L(+) arginine was not detected in the presence of D(+) arginine or homoarginine. Citrulline was the only exception among the arginine-related amino acids; it displayed neither stimulatory nor inhibitory potency on glucagon release. The A2-cell response to D(+) amino acids and artificial analogues of arginine is a strong case for the theory of amino acid receptors' triggering the release of the hormone before (or in the absence of) further metabolism. The prominent rank of arginine and ornithine amont stimulatory amino acids and some other physiologic evidence suggest that A2-cell may play a regulatory role in the metabolsm of ammonia by the liver.

Amino Acids↗
PubMed1977

Hormonal and metabolic effects of somatostatin in diabetic patients submitted to an i.v. arginine infusion.

Hormonal and metabolic effects of a synthetic linear somatostatin were tested in insulin-dependent subjects submitted to an intravenous arginine infusion. Arginine alone induced a rise in plasma growth hormone (HGH) and glucagon (IRG) concentrations but did not affect the spontaneous diurnal decrease of plasma cortisol; blood glucose concentration rose while that of alanine decreased suggesting enhanced gluconeogenesis; concentrations of plasma free fatty acids (FFA) and 3-hydroxybutyrate decreased. Somatostatin, at three different dosages, markedly influenced these patterns: HGH response to arginine was suppressed by the lowest somatostatin dose; IRG response was progressively inhibited by increasing doses of somatostatin but never reached zero; cortisol level was not decreased but slightly increased by somatostatin. Substrate responses to arginine were also modified by somatostatin: alanine disappearance was impaired, this effect being dose-related; plasma FFA and 3-hydroxybutyrate concentrations showed a significant increase rather than decrease, consistent with somatostatin suppression of residual insulin secretion. Tolerance to somatostatin was good and no alteration of hemostasis was observed.

Adult↗
PubMed1977

Reliability of a simple and rapid glucose measuring device in conducting oral glucose tolerance tests.

160 oral glucose tolerance tests (OGTTs) were carried out, the glucose measurements being performed with the rapid dry-lab device Reflomat/Reflotest-Glucose and the GOD-Perid method. In 151 patients (94.4%) the two methods of measuring glucose led to the same diagnoses (i.e. "normal", "suspect" or "diabetic"). This high conformity in the results suggests the reliability of the rapid device in conducting OGTTs. Only in 9 subjects (5.6%) were the clinical conclusions different, Reflotest-Glucose giving predominantly "more pathological" results. It is, however, not possible to say which method showed "falsely positive" and which one "falsely negative" results.

Blood Glucose↗
PubMed1976

Total pancreatectomy in the treatment of acute necrotising and hemorrhagic pancreatitis. Indications-technique.

The place of total pancreatectomy in the treatment of pancreatitis is still not clear: the author is in favour of this operation and gives the indications, surgical technique, complications and results. The operation is indicated in cases of necrosis involving more than 2/3rds of the whole of the head and part of the body of the pancreas. The duodenum and pancreas should be removed in one piece and intestinal continuity should be restored performing choledocho-jejunal and gastro-jejunal anastomoses. It is important to carry out this operation early, between the 3rd and 6th days, treating all areas of necrosis before the lesions become the site of uncontrollable infection. Seven patients out of 9 are still alive, on the 25th of July 1975; they all have easily controlled diabetes, a low fat diet and are receiving pancreatic extract. We have recently operated a 10th case, and the patient is alive 2 months later.

Acute Disease↗
PubMed1976

Effects of exogenous hormones and glucose on plasma levels and hepatic metabolism of amino acids in the fetus and in the newborn rat.

The present study examines the role of insulin, glucagon and cortisol in the regulation of gluconeogenesis from lactate and amino acids in fetal and newborn rats. Injection of glucagon in the full-term fetal rat caused a rise in glucose (and insulin) and a fall in blood levels of most individual amino acids, stimulated hepatic accumulation of 14C-amino isobutyric acid and 14C-cycloleucine and increased the conversion of 14C lactate, alanine and serine to glucose in vivo and in vitro (liver slices). Such changes were equivalent to the changes seen in 4 h old newborn rats. When glucagon was administered at birth, little difference was observed between control and treated animals in plasma amino acids and a smaller increment in conversion of 14C substrate to glucose occurred. By contrast, insulin injection at birth caused hypoglycemia, suppression of levels of certain amino acids and inhibition of conversion of 14C substrates into glucose. Glucose injection at birth caused elevated glycemia and plasma insulin and suppression of most amino acid levels and of conversion of 14C substrate into glucose. Cortisol injection at birth caused a marked, generalized by hyperaminoacidemia, a stimulation of glucagon secretion and of conversion of 14C substrates into glucose. These observations support the thesis that glucagon plays a major role in the induction of hepatic gluconeogenesis and that insulin acts as an antagonist hormone.

Amino Acids↗
PubMed1976

Studies on experimental hypotrophy in the rat. III. Plasma insulin and glucagon.

Insulin and glucagon have been measured in the plasma of rats with intrauterine growth retardation (IUGR) and their littermate controls. A lower plasma insulin and a higher plasma glucagon were observed in IUGR term rat fetuses. After birth there was no difference in the circulating level of insulin and glucagon in IUGR rats and their littermate controls. It is concluded that postnatal hypoglycemia of IUGR rat did not result from an impaired glucagon secretion or an increased insulin secretion.

Age Factors↗
PubMed1976

Effect of environmental temperature on glucose-induced insulin response in the newborn rat.

Blood glucose and plasma insulin and glucagon concentrations were determined in full-term rats delivered by cesarean section and exposed to 37 degrees C. or 24 degrees C. environmental temperature during the first hours of extrauterine life. When newborn rats were maintained at thermal neutrality (37 degrees C.), a transient period of hypoglycemia of two hours occurred, associated with a rapid fall in plasma insulin and a rise in plasma glucagon concentrations. During cold exposure (24 degrees C.), the blood glucose level remained stable over the four hours studied; the decrease of plasma insulin was sluggish while the rise of plasma glucagon was unchanged. In newborn rats maintained at 37 degrees C., an intraperitoneal glucose load one hour after delivery produced a marked rise in blood glucose and plasma insulin concentrations one hour later. The distribution of experimental points suggested a sigmoidal dose-response curve. By contrast in newborn rats kept at room temperature (24 degrees C.) the same glucose load did not induce any increase in plasma insulin in spite of hyperglycemia. However, phentolamine resulted in pronounced plasma insulin rise in hypothermic newborns in response to glucose administration. From these observations it is concluded that the in-vivo unresponsiveness of the beta cells to glucose at birth, reported by others, is mainly due to the experimental conditions.

Age Factors↗
PubMed1976

[Somatostatin, a new hormone? (author's transl)].

Somatostatin, or SRIF (Somatotropin Release Inhibiting Factor), is a tetradecapeptide of hypothalamic origin, which inhibits the secretion of growth hormone. It has also been recognized in other parts of the central nervous system, in the islets of Langerhans, and the mucosa of the upper digestive tract. Parenteral administration of synthetic SRIF inhibits the release of growth hormone, basal and stimulated by muscular exercise, arginine, L-DOPA, insulin-induced hypoglycemia, and sleeping. It also inhibits insulin and glucagon secretion, basal and stimulated, and several other secretory processes in endocrine and exocrine glands. It may have a depressor effect on some neurons in the central nervous system. Considerable interest has been prompted in the field of diabetology by the demonstration of somatostatin-induced suppression of growth hormone and glucagon : both hormones are over-secreted in many diabetic patients, and both may be noxious for small blood vessels in the diabetic. The eventual therapeutic use of somatostatin in humans is restricted, for the moment, by the unavaibility of long-acting SRIF preparations and the possibility of some adverse effects mainly affecting hemostasis. Evaluation of the physiological role (s) for this newcomer, and of the eventual pathophysiology of endogenous somatostatin, represent an unexpected and exciting field of neuro-endocrinology.

Amino Acid Sequence↗