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At least 19 recordsLinked to original sources
PubMed1975

The effects of D- and L-glyceraldehyde on glucose oxidation, insulin secretion and insulin biosynthesis by pancreatic islets of the rat.

D-glyceraldehyde stimulated insulin secretion from isolated rat pancreatic islets in static incubation and perifusion systems. At low concentrations (2-4 mM) D-glyceraldehyde was a more potent secretagogue than glucose. The insulinotropic action of 15 mM D-glyceraldehyde was not affected by D-mannoheptulose, was potentiated by cytochalasin B (5 mug/ml) and theophylline (4 mM), and was inhibited by both adrenalin (2 muM) and somatostatin (10 mug/ml). D-glyceraldehyde at a concentration of 1.5 mM produced a 10-fold increase of L-[4,5-3H]leucine incorporation into proinsulin and insulin without a significant increase into other islet proteins. Glucose at 1.5 mM did not stimulate proinsulin biosynthesis. D-Glyceraldehyde at concentrations higher than 1.5 mM, in marked contrast to glucose, progressively inhibited incorporation of labelled leucine into proinsulin + insulin and other islet proteins. D-Glyceraldehyde also inhibited the oxidation of glucose. L-Glyceraldehyde did not stimulate proinsulin biosynthesis and had less effect than the D-isomer on insulin release and glucose oxidation. The results strongly suggest that metabolites below D-glyceraldehyde-3-P are signals for insulin biosynthesis and release. Interaction of D-glyceraldehyde with a "membrane receptor" cannot, however, be excluded with certainty.

Animals↗
PubMedDate not supplied

Relationship between carbohydrate tolerance, insulin secretion, and insulin sensitivity of isolated fat cells from obese protodiabetics.

Six normal weight subjects without any heredity of diabetes (group 1), 3 obese subjects with normal (group 2) and 9 with pathological carbohydrate tolerance (group 3) were characterized by a 2-h glucose infusion test. Adipose tissue fragments were obtained from the abdominal wall by surgical biopsy under intracutaneous anesthesia. Adipocytes were isolated by collagenase digestion and incubated in buffer containing [1-14C] glucose and different concentrations of insulin. The metabolic effect of insulin was expressed as percent increase above control 14CO2 production. Maximal CO2 raised to 207 +/- 25% and 154 +/- 9% in groups 1 and 2, respectively. These values were significantly higher than in obese subjects displaying a pathological carbohydrate tolerance (group 3; 119 +/- 6%). A negative correlation was found between blood glucose levels and biological activity of insulin on adipocytes. The results suggest that insulin sensitivity of target tissue seems to play an important role in development of carbohydrate intolerance.

Adipose Tissue↗
PubMed1976

Investigations on isolated islets of Langerhans in vitro. XIV. Insulin secretion and insulin stores of cultivated islets from sand rats (Psammomys obesus): investigations of glucose-dose response.

Release of immunoreactive insulin activity (IRI) and biological insulin like activity (ILA) from collagenase isolated pancreatic islets of sand rats (Psammomys obesus) maintained on a vegetable diet were examined at 60 min and 24-48 h intervals under culture conditions at 1.0 and 15.6 mM glucose. The glucose-insulin dose response curves for sand rats after 60 min incubation were compared with those after 24 or 48 h of incubation. The pancreatic islets responded to 5mM glucose with a high insulin release especially under culture conditions. A drastic depletion of stored insulin in the islets cultivated for 2 days at 5 or 15 mM glucose is accompanied by a continuous diminution of the glucose-induced insulin release with the prolongation of cultivation up to one week.

Animals↗
PubMed1976

Glucose-induced insulin secretion and insulin sensitivity of peripheric organs of Egyptian sand rats before manifestation of diabetes.

In Egyptian sand rats (Psammomys obesus) fed with native food and a low caloric vegetable diet after capture it was possible to study endocrinologic and metabolic changes of the early stages during the progression to diabetes. According to body weight gain and fasting blood glucose the animals were differentiated into two groups classified as basic and protodiabetic group, respectively. Isolated pancreatic islets as well as the perfused pancreases of sand rats responded to low concentrations of glucose with high insulin release during early stages of the development to diabetes. Changes in the insulin content of the islets could not be detected at this time although in the B-cells of the protodiabetic animals a degranulation was visible. During these early stages of the development to diabetes the in vitro insulin action on glucose utilization in soleus muscle and especially in epididymal fat pads as well as the basal glucose metabolism in adipose tissue were low. This strikingly reduced utilization of glucose by adipose and muscle tissues may be a factor which challenges the B-cell.

Adipose Tissue↗
PubMed1977

Insulin secretion in insulin-requiring diabetics before and during insulin treatment.

Endogenous insulin secretion after different stimuli was determined in insulin requiring diabetics without circulating insulin antibodies. Four groups of non-obese diabetics were investigated and compared with 111 controls. Group I: 14 patients with mild diabetes, not yet requiring insulin; diagnosis before the age of 30 years. Group II: 19 ketonuric patients just before being started on insulin treatment. Group III: 18 patients during remission after an average of 16.5 months' insulin treatment. Group IV: 13 patients with no remission period or relapse after an average of 19.5 months on insulin treatment. Blood glucose and immunoreactive insulin were measured during fasting and after iv secretin, iv tolbutamide, iv GTT, and oral GTT, followed by combined iv tolbutamide and glucagon stimulation. A considerable insulin secretion could be demonstrated in group I, whereas in group II only a very low insulin peak was obtained after secretin and the combined injection of glucagon and tolbutamide. In group III considerable insulin secretion was demonstrated, whereas in group IV only a very low insulin peak was obtained. A significant correlation between the degree of metabolic control and endogenous insulin secretion was found.

Adult↗
PubMed1979

Insulin secretion and peripheral insulin sensitivity in obese children. Evidence of deficient glucose-stimulated early insulin release despite hyperinsulinemia.

Insulin secretion and peripheral insulin sensitivity were studied in 19 grossly-obese girls and 17 age-matched non-obese girls by means of the intravenous glucose tolerance test (IVGTT) and the simulated early insulin response test (SERT) respectively. SERT measures the fall in fasting blood glucose after a short infusion of insulin, performed so as to simulate the early phase of insulin release to the acute stimulus of an intravenous glucose load (ERex). In the IVGTT, the obese girls showed significantly increased early insulin response (ERend) in comparison with the non-obese girls. The glucose disappearance rate (KG) was similar in the two groups, although four obese girls had borderline low values. In the SERT, the rise in plasma insulin caused a much smaller decrease in blood glucose in the obese girls, than in the reference girls over the whole range of insulin levels studied. The relationship between insulin sensitivity and insulin secretion of each subject was evaluated from the plot of the ERex/ERend ratio vs blood glucose decrement. This showed that the hyperinsulinemia of the obese girls did not match the degree of peripheral resistance.

Blood Glucose↗
PubMed1979

Effects of pregnancy and progesterone and/or oestradiol on the insulin secretion and pancreatic insulin content in the perfused rat pancreas.

Progesterone and oestradiol treatment of ovariectomized rats was administered leading to plasma steroid concentrations comparable to those of the pregnant rat. In these experimental conditions oestradiol enhanced insulin secretion but progesterone had little effect on B cell response to glucose (0.8 g/l and 1.4 g/l) of the perfused pancreas. At low glucose concentration (0.8 g/l) neither of the two steroids, added to the perfusion medium, had any effect on insulin release of the pancreas of the castrated animals; oestradiol exerted a facilitating action on glucose stimulation (1.4 g/l); progesterone had no effect. During pregnancy biphasic insulin secretion was enhanced, but pancreatic hormonal content was only increased at term. Neither oestradiol nor progesterone treatment changed pancreatic insulin content. It is concluded that oestradiol acts on insulin release at pancreatic level directly, whereas progesterone influences insulin release by causing insulin resistance.

Animals↗
PubMed1976

Enhancement of insulin secretion by human chorionic somatomammotropin and related hormones.

Hypophysectomized rats were treated for 6 days with 200 mug per day of either human chorionic somatomammotropin, human pituitary growth hormone, plasmin-modified human pituitary growth hormone, or ovine prolactin. All hormone preparations except ovine prolactin enhanced the ability of the pancreases of hypophysectomized rats to secrete insulin in the isolated pancreas perfusion system.

Animals↗
PubMed1975

[The effect of preparative pancreatic digestion with collagenase on the glucose stimulated insulin secretion of isolated Langerhans islets].

Pancreatic islets of wistar rats, isolated after 15 min of digestion with collagenase, secreted insulin in response to 15.0 mM glucose within 2 min and showed the typical sigmoidal glucose response during an incubation time of 15 and 60 min, respectively. Islets, isolated after 35 min of digestion with collagenase, responded with delay after stimulation with glucose (after 15 min of incubation), and are characterized by an increased "release" in the presence of 2.5 mM glucose.

Animals↗
PubMed1977

An appraisal of radical pancreatoduodenectomy based on insulin secretion.

The effect of pancreatoduodenectomy on insulin secretion was determined in seven patients with periampullary malignant tumors. As a uniform stimulus for secreting insulin, 100 gm of glucose was administered orally to all patients and glucose tolerance tests were carried out. Glucose intolerance and poor insulin secretion were obvious both pre- and postoperatively. Indexes of an initial insulin response, of a maximum insulin increment, and of total secretion of insulin responding to the stimulus of glucose were significantly lower in these patients before and after pancreatoduodenal resection, as compared with normal subjects. It was also observed that these three indexes, which express the ability of the pancreas to secrete insulin, decreased without exception after pancreatoduodenectomy. In light of these data it is postulated that radical pancreatoduodenectomy further diminishes the already insufficient secretion of insulin indicated by the oral glucose tolerance test in patients with periampullary malignant tumors.

Adolescent↗
PubMed2024

Whole transcriptome sequencing analyses of islets reveal ncRNA regulatory networks underlying impaired insulin secretion and increased β-cell mass in high fat diet-induced diabetes mellitus.

AIM: Our study aims to identify novel non-coding RNA-mRNA regulatory networks associated with β-cell dysfunction and compensatory responses in obesity-related diabetes. METHODS: Glucose metabolism, islet architecture and secretion, and insulin sensitivity were characterized in C57BL/6J mice fed on a 60% high-fat diet (HFD) or control for 24 weeks. Islets were isolated for whole transcriptome sequencing to identify differentially expressed (DE) mRNAs, miRNAs, IncRNAs, and circRNAs. Regulatory networks involving miRNA-mRNA, lncRNA-mRNA, and lncRNA-miRNA-mRNA were constructed and functions were assessed through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. RESULTS: Despite compensatory hyperinsulinemia and a significant increase in β-cell mass with a slow rate of proliferation, HFD mice exhibited impaired glucose tolerance. In isolated islets, insulin secretion in response to glucose and palmitic acid deteriorated after 24 weeks of HFD. Whole transcriptomic sequencing identified a total of 1324 DE mRNAs, 14 DE miRNAs, 179 DE lncRNAs, and 680 DE circRNAs. Our transcriptomic dataset unveiled several core regulatory axes involved in the impaired insulin secretion in HFD mice, such as miR-6948-5p/Cacna1c, miR-6964-3p/Cacna1b, miR-3572-5p/Hk2, miR-3572-5p/Cckar and miR-677-5p/Camk2d. Additionally, proliferative and apoptotic targets, including miR-216a-3p/FKBP5, miR-670-3p/Foxo3, miR-677-5p/RIPK1, miR-802-3p/Smad2 and ENSMUST00000176781/Caspase9 possibly contribute to the increased β-cell mass in HFD islets. Furthermore, competing endogenous RNAs (ceRNA) regulatory network involving 7 DE miRNAs, 15 DE lncRNAs and 38 DE mRNAs might also participate in the development of HFD-induced diabetes. CONCLUSIONS: The comprehensive whole transcriptomic sequencing revealed novel non-coding RNA-mRNA regulatory networks associated with impaired insulin secretion and increased β-cell mass in obesity-related diabetes.

Mice↗
PubMed1975

Glucose tolerance and insulin secretion in patients with parathyroid disorders. Effect of serum calcium on insulin release.

To evaluate the role of serum calcium in human insulin secretion, insulin responses after a 100-g oral glucose load were studied in nine patients with primary hyperparathyroidism, five with idiopathic hypoparathyroidism, three with pseudohypoparathyroidism and one with normocalcemic secondary hyperparathyroidism. Glucose tolerance values in these disorders were almost normal. Insulin responses in primary hyperparathyroidism were increased, and those in idiopathic hypoparathyroidism and pseudohypoparathyroidism were reduced significantly as compared to normal subjects. Isulin response in secondary hyperparathyroidism was normal. The calculated insulin area during an oral glucose load was significantly correlated with serum calcium (5.1 to 12.2 mg per deciliter), and a linear relation was obtained (y = 1.59x - 3.3, r = 0.81, p less than 0.001), although a relation with the glucose area was not found. These observations indicate that serum calcium has an important effect on insulin secretion in parathyroid disorders.

Calcium↗
PubMed1975

Feed-back inhibition of insulin secretion in subjects with high and low insulin response to glucose.

The plasma insulin response to two successive stimulations by glucose was measured in 12 healthy subjects, 5 of whom demonstrated subnormal insulin responses to glucose infusion (low insulin responders). 15 g of glucose were injected rapidly i.v. at 0 and 20 min, and blood glucose and plasma insulin levels determined at intervals of 2-10 min. In both groups, the peak elevation of plasma insulin, and the peak insulinogenic index, were significantly inhibited at the second stimulation. The degree of inhibition was smaller in subjects with low insulin response. The integrated insulin response and the integrated insulinogenic index during the 20 min following glucose administration were also significantly inhibited at the second glucose challenge in subjects with low insulin responders. The degree of inhibition of the second insulin response (20-40 min) shows significant correlation with the insulinogenic index of the first response (0-20 min) in the total material. It is suggested that this inhibition of insulin release on repeating the stimulus, (a) may offer an explanation sustained stimulation by glucose; (b) is probably generated by the phenomenon of insulin secretion, and (c) might thus represent a negative feed-back loop in insulin secretion. (d) Decreased insulin secretion in low responders is not due to the presence of increased inhibition.

Adult↗