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At least 19 recordsLinked to original sources
PubMed2026

Duration and characteristics of hypoglycemia with once-weekly insulin efsitora alfa versus once-daily basal insulins in adults with type 2 diabetes: Exploratory safety analysis of QWINT 2-4.

AIMS: Efsitora is a novel once-weekly basal insulin. Efsitora demonstrated similar efficacy and safety compared with once-daily basal insulin comparators across four phase 3 clinical trials for type 2 diabetes. This exploratory safety analysis further characterizes hypoglycemia events in the efsitora and once-daily treatment groups in three of these trials (QWINT-2, -3, and -4). METHODS: Median duration of hypoglycemia events was assessed with masked continuous glucose monitoring. Incidence of persistent-recurrent (PR) hypoglycemia was assessed by investigators and by a pre-specified algorithm using SMBG e-diary data. Factors contributing to hypoglycemia, characteristics of hypoglycemia, and treatment methods were reported by participants and assessed across groups. RESULTS: Across the three trials, durations of hypoglycemic events for efsitora vs once-daily basal insulin comparators were: Level 1 and 2 [<70&#xa0;mg/dL]: 40-42.5 vs 40&#xa0;min; Level 2 [<54&#xa0;mg/dL]: 35-39.9 vs 35&#xa0;min. Few incidences of PR hypoglycemia were reported for efsitora or once-daily comparators. No major descriptive differences were observed between hypoglycemia contributing factors, characteristics, or treatment methods in efsitora and once-daily treatment groups. CONCLUSIONS: No clinically relevant differences were observed between the duration or characteristics of hypoglycemic events in efsitora and once-daily treatment groups in the QWINT-2, -3, and -4 trials.

Adult↗
PubMed1977

Suppression of basal insulin secretion by adrenalin in normal man and in patients with insulinomas.

Basal insulin secretion has been thought to be via a different mechanism from stimulated insulin secretion, partly because it is not similarly suppressed by adrenalin. However, adrenalin normally causes hyperglycaemia, but if it is infused while the plasma glucose is kept constant there is marked suppression of insulin secretion. Sympathetic stimulation modulates basal insulin secretion, and alpha adrenergic blockade impaired the suppression of insulin secretion in response to hypoglycaemia. Four of five benign insulinomas had marked suppression of insulin secretion by adrenalin, but one malignant and one benign insulionoma had little suppression. Both had a raised proportion of their basal plasma insulin as proinsulin, and the impaired suppression of secretion by adrenalin probably signified an undifferentiated tumour.

Adenoma, Islet Cell↗
PubMed1978

Influence of basal insulin and glucagon secretion on potassium and sodium metabolism. Studies with somatostatin in normal dogs and in normal and diabetic human beings.

To examine the role of basal insulin and glucagon secretion in potassium and sodium homeostasis, somatostatin, a potent inhibitor of insulin and glucagon secretion, was infused for 5 h into healthy human subjects, maturity-onset diabetes, juvenile-onset diabetics, and normal dogs. Infusion of somatostatin resulted in an increase in serum potassium (0.5-0.6 meq/liter) in normal subjects and maturity-onset diabetics, but not in juvenile-onset diabetics despite equivalent reductions in plasma glucagon in all three groups. A similar rise in serum potassium was observed in normal conscious dogs given somatostatin and was reversed by insulin replacement. Urinary excretion of potassium was unaffected by somatostatin. In dogs given intravenous potassium chloride in doses (0.375 meq/kg per h) which do not alter basal insulin levels, the rise in serum potassium (0.6 meq/liter in controls) increased 100% when somatostatin was administered together with the KCl infusion. Addition of replacement doses of insulin to the somatostatin infusion resulted in increments in serum potassium which were comparable to infusion of KCl alone. Urinary potassium excretion rose after KCl administration and was unchanged by the addition of somatostatin. Serum sodium concentration was unaffected by somatostatin administration in both the human and dog studies. However, urinary sodium excretion displayed a biphasic response falling by 20-60% within the first 2 h of somatostatin administration and then rising to values 50-80% above basal levels at 3-4 h. Inulin and p-aminohippurate clearances were unaffected by somatostatin. It is concluded that (a) potassium homeostasis is influenced by basal insulin levels in the absence of which serum potassium concentration rises and potassium tolerance declines; (b) this effect of insulin is mediated via extrarenal mechanisms of potassium disposal; (c) somatostatin has a biphasic effect on urinary sodium secretion, the mechanism of which remains to be established.

Adult↗
PubMed1975

Effect of force-feeding upon basal insulin levels of rats.

Rats were over- or under-fed to achieve a wide range of body weights. The effect of this treatment on basal insulin levels, with and without pretreatment with atropine, was examined. Basal insulin was positively correlated with body weight and this relationship was essentially unchanged in the presence of atropine.

Animals↗
PubMed1977

Counter regulation of basal insulin secretion during alcohol hypoglycemia in hypercalcemic and normocalcemic man.

In seven normocalcemic subjects, fasted for 48 hours, alcohol hypoglycemia has been accompanied by a significant decline in basal insulin secretion. In another six healthy subjects, fasted for two days, infusion of calcium also induced a significant fall in basal secretion of insulin. However, when six healthy volunteers, fasted for two days, were infused with calcium and given alcohol simultaneously, no significant fall in insulin was recorded, even though the hypoglycemia, following this combined load, was of the same magnitude as in the subjects given alcohol alone. The implications of these findings are discussed.

Adult↗
PubMed1977

Glucose control of basal insulin secretion in diabetes.

The plasma insulin response to both a small increase and decrease in the plasma glucose has been studied in normal and diabetic, non-obese subjects. In a second investigation the plasma insulin concentrations were measured during a gradual reduction of the raised fasting plasma glucose of diabetes to normal levels. In both studies, diabetic patients were found to have a markedly impaired response of the fasting plasma insulin to small changes in plasma glucose. These results do not support the suggestion that stimulated and not basal insulin secretion is impaired in diabetes. Both modes of secretion are probably via the same B-cell release mechanism, which is deficient in diabetes. There was a gradation of response between maturity onset and juvenile onset diabetics.

Aged↗
PubMed1977

Effect of caloric restriction on basal insulin levels and the in vivo lipogenesis and glycogen synthesis from glucose in the Koletsky obese rat.

Fasting plasma immunoreactive insulin levels increased with age in hyperinsulinemic Koletsky obese rats, being almost four times as high as in lean siblings at 3 mo (40 +/- 5 muU/ml) and rising steadily to 82 +/- 4 muU/ml at 6 mo (about seven times higher than lean siblings). Restricting the food intake of the obese rats markedly reduced but did not normalize the hyperinsulinemia, which in these rats was accompanied by normal plasma glucose concentrations. The incorporation in vivo of D-U-14C-glucose into tissue lipids and glycogen was measured 1 hr after the intravenous injection of 1 g glucose (containing 100 muDi D-U-14C-glucose) per kg body weight in obese rats eating ad libitum, obese rats after 3 mo on a restricted food intake, and lean siblings. All tissues (heart, diaphragm, skeletal muscle, and adipose tissues and liver) of obese rats exhibited a significantly greater lipogenesis from glucose than those of lean siblings. Dietary restriction of the obese rats reduced the 14C incorporation into lipid to levels not significantly different from lean controls in all tissues except skeletal muscle and liver, where, although greatly reduced, lipogenesis was still significantly higher than in lean rats. Glycogen synthesis tended to be greater in all tissues of obese rats than in lean animals. Dietary restriction of obese rats did not greatly affect glycogen synthesis.

Animals↗
PubMed1976

Insulin rather than glucose homoeostasis in the pathophysiology of diabetes.

Hepatic glucose efflux is very sensitive to changes in plasma-insulin and it is postulated that this provides an important feedback control of insulin secretion. In diabetes this hepatic "insulin sensor" increases the basal plasma-glucose until the impaired beta cells are sufficiently stimulated to secrete normal basal insulin concentrations. Glucose regulation thus becomes of secondary importance to the maintenance of basal insulin secretion, which is teleologically needed for the "anabolic" requirements of cell growth. This hypothesis provides an explanation for the "normal" basal plasma-insulin concentrations found in diabetes in spite of impaired beta-cell function. This maintenance of basal insulin secretion accounts for the discrepancy between the marked hyperglycaemia and minimal ketosis of maturity onset diabetic patients.

Diabetes Mellitus↗
PubMed1979

Alterations of the basal serum insulin and blood glucose in brain-injured patients.

Serial fasting blood glucose and basal serum insulin were measured in brain-injured patients. The endocrine changes were compared with the level of consciousness. Evaluating the serial examinations of 92 brain-injured and 31 control patients we came to the following conclusions. There is a quantitative correlation between the alterations in the level of consciousness and the fasting blood-glucose and serum-insulin levels in brain-injured patients. Deep coma is connected with a high blood-sugar level, clear consciousness with a normal glucose level. The insulin level is, however, decreased in the comatose state and normal in the state of clear consciousness. According to the alterations in blood-glucose and insulin levels, brain-injured patients can be divided into four groups. The alterations in the insulin level cannot give a proper explanation of the blood-sugar changes. Some changes in the levels of both blood glucose and serum insulin may have prognostic significance. According to our results it can be supposed that certain cerebral structures take part in the regulation of the basal insulin secretion.

Blood Glucose↗
PubMed1979

Insulin deficiency and insulin resistance interaction in diabetes: estimation of their relative contribution by feedback analysis from basal plasma insulin and glucose concentrations.

The liver and beta cells function in a negative feedback loop, which appears to have a predominant role in regulating both the basal plasma glucose and insulin concentrations. The degree of basal hyperglycemia in diabetes probably provides a bioassay of both the effect of a reduction in insulin secretory capacity and the degree of insulin resistance. A mathematic model of the interaction of insulin deficiency and insulin resistance has been constructed, based on the known response characteristics of the beta cells to glucose, and of plasma glucose and insulin control of hepatic and peripherpal glucose flux. The degree to which beta cell deficiency increases basal plasma glucose reflects the hyperbolic shape of the normal insulin secretory response to different glucose concentrations. The height of basal plasma insulin is a function of the degree of insulin resistance. From the basal plasma insulin and glucose concentrations, the model provides an estimate of the degree to which both beta cell deficiency and insulin resistance contribute to diabetes. The predictions arising from the model are in accord with experimental data in man and in animals. In normal-weight diabetics who do not have increased insulin resistance, the model predicts that more than 85% of beta cell function has to be lost for the basal plasma glucose to rise to 6 mmol/liter, but a further 5%--10% loss increases the basal plasma glucose to over 10 mmol/liter. In a third of a consecutive series of 65 newly presenting, uncomplicated diabetics, both normal weight and obese, the analysis from the model suggested that insulin resistance, rather than beta cell deficit, was the predominant feature.

Blood Glucose↗
PubMed1978

Insulin secretion in fetal and newborn sheep.

The relationships between arterial plasma insulin, glucose, and fructose concentrations during the fed and fasted state were studied in seven fetal lambs and their mothers. A significant correlation between insulin and glucose concentration was noted in all fetal lambs and in their mothers. Fetal sensitivity to glucose, as measured by the slopes of the insulin-response curves, was equal to that of the adult although the fetal response was shifted to the left of the maternal. Glucose infusion in four fetal lambs caused significant insulin elevations but no early insulin response (phase I). Maternal fasting caused no alteration in glucose-induced response in the fetus. Similar glucose infusions in newborn and 1-mo-old lambs demonstrated significant early-phase insulin secretion. Basal insulin to glucose ratios were consistent with an adult pattern as early as 3 days after birth.

Animals↗
PubMed1975

The effect of insulin on basal and hormone-induced elevations of cyclic AMP content in cultured human fibroblasts.

Studies were carried out on confluent cultures of human fibroblasts to explore the effect of insulin on basal and hormone-induced elevations of intracellular cyclic AMP content during short-term incubations in serum-free medium. Insulin tended to decrease basal levels of cyclic AMP but this was not statistically significant. Similarly, insulin was unable to block the elevations of intracellular cyclic AMP content induced by PGE1, epinephrine and glucagon. Paradoxically, when cells were preincubated with insulin, PGE1-stimulated cyclic AMP elevation was potentiated, possibly because insulin was conserving factors needed for a maximal PGE1 stimulus or retarding the leakage of cAMP itself. The results indicate that insulin has little or no direct effect on cyclic AMP metabolism in cultured human fibroblasts and is consistent with the known insensitivity of these cells to insulin for other parameters.

Adult↗
PubMed1976

Effect of heparin on insulin secretion in vivo and in vitro.

The effect of heparin of therapeutic dose on the basal insulin secretion and on that of induced by glucose stimulation was studied in dogs and in Langerhans islets in vitro model. The effect of heparin, given intraarterially (a. pancreaticoduodenalis sup.) and injected i.v. before i.v. glucose load, on the immuno-reactive insulin concentration of the pancreatic and peripheral venous blood as well as the blood sugar and free fatty acid levels of the peripheral venous blood was investigated. Heparin inhibited significantly both the basal insulin secretion and that of following glucose stimulation. After the injection of heparin the glucose assimilation coefficient decreased significantly. The inhibitory effect of heparin on the basal insulin secretion and the glucose stimulated insulin secretion was observed in Langerhans islets in vitro model, too. This suggests that heparin, at least partly, inhibits insulin secretion directly through its influence on the beta cells.

Animals↗
PubMed1977

[Serum insulin concentration, basal and during an standardized oral glucose tolerance test in healthy children (author's transl)].

Serum insulin concentration was measured, basal and during an standardized oral glucose tolerance test in 110 healthy children. The patients are divided in four groups according to their pediatric ages. The method used to measure serum insulin was a radioimmunoassay and the glucose by oxidative enzymatic procedures. The calculations of the results has been made with log-conversion in order to follow a normal log distribution of the data. Glucose, insuline areas and some insulinogenic index (ratio) are made as well. And relations of multiple correlations. With our results we can conclude: There is a general tendency in all our cases to low values of insulin most marcate in the fasting levels. We defined like hiposecretor the 4.1% of all our patients. The existence of a positive correlation between insuline-age in fasting determinations as well as in overload test.

Adolescent↗