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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A basic understanding of fetal nutrition and metabolism is essential in the clinical management of the obstetric patient. The fetus depends upon a constant infusion of glucose for energy production and growth. Maternal glucose is the prime source of this nutrient. Alterations in maternal carbohydrate homeostasis will lead to changes in fetal metabolism. In diabetes mellitus, hyperglycemia may produce hyperinsulinemia and macrosomia. The growth-retarded fetus may have a decreased supply of maternal glucose and reduced amounts of hepatic glycogen and adipose tissue. The fetus must depend upon these stores for survival during periods of intrauterine hypoxia. In the newborn period, hypothermia and hypoxia may rapidly deplete energy reserves. With this information, the clinician may more knowledgeably manage dietary demands in the antepartum patient, fetal distress during labor, and the immediate newborn period.
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PMID:Fetal carbohydrate metabolism: its clinical importance. 31 3

A patient with obesity and diabetes mellitus had insulin secretion studies done during a 3-year cycle of weight loss and regain in the course of which she progressed from frank diabetes to a normal state of carbohydrate tolerance and then back to her original diabetic state. The results suggest that therapeutic weight reduction not only reverses insulin resistance but also restores beta cell sensitivity and enhances beta cell capacity. The eventual re-establishment of a degree of obesity, hyperinsulinemia, and carbohydrate intolerance virtually identical to that originally seen is compatible with a primary disorder involving hypothalamic control of adipose stores and insulin secretion.
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PMID:Insulin secretion in obesity and diabetes: an illustrative case. 33 68

The long-term effects of sulfonamides were studied by means of hyperinsulinemia tests in 82 diabetics over a period of 12 months (24 months for 30 of them). Whereas for those (obese) diabetes whose only treatment was dieting--alone or combined with biguanides--hyperinsulinemia attenuates itself as do also variations in glycemia, although some asynchronism remains, in those diabetics treated with sulfonamides--alone or in combination with other treatments--the insulinemia curve is hardly modified.
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PMID:[Long term course of insulin secretion in treated non-insulin dependent diabetics (author's transl)]. 35 1

Obesity in the Zucker rat is accompanied by hyperlipemia, hyperinsulinism, insulin resistance, pancreatic hyperplasia, and islet hypertrophy. This study correlates the morphologic heterogeneity of isolated pancreatic islets with secretion of insulin and glucagon in the perifusion system. Islet size was arbitrarily defined as large (greater than 0.45 mm) or small (smaller than 0.12 mm). Protein content and volume (V = 4/3pir3) were calculated for groups and individual islets, respectively. Islets from obese rats secreted more insulin in response to glucose and aminophylline than islets from lean rats (peak 7.8 +/- 2.4 vs. 1.5 +/- 0.37 microU/islet/min, P less than 0.005). Insulin release was related directly to islet size and protein content. Small islets from lean and obese animals produced less insulin per islet than large islets (P less than 0.005). In terms of islet volume, however, large islets were inefficient insulin releasers as compared to small islets (P less than 0.005). Stimulation with Br-cAMP released glucagon from islets of lean but not from large islets of obese animals (peak 11 +/- 3.3 vs. 4.1 +/- 0.3 pg/microgram protein per minute, P less than 0.05). Arginine produced the same effect on glucagon release (P less than 0.05) as stimulation with Br-cAMP. The observed increased insulin release rates and the blunted glucagon response are related to islet size in the pancreas of the Zucker rat.
Diabetes 1979 Jun
PMID:Correlation between morphology and function in isolated islets of the Zucker rat. 37 79

We have demonstrated how in psoriasis, irrespective of any diabetic family history, there exists a state of hyperinsulinism with a decreased resistance to insulin, which is aggravated by obesity. Since reviewing the latest studies concerning diabetes at the receptor level, we have carried out a comparative study dealing with insulin receptors in lymphocytes in homogeneous groups of normal, obese, and psoriatics of normal weight and overweight. We have also made a comparison regarding the behaviour of the receptors in these various metabolic states.
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PMID:Insulin receptors in psoriasis. 39 47

Physiopathological basis and methodological implications of the radioimmunological estimation of plasma C-peptide, as a test of beta cell secretory activity, are reviewed. Personal results are reported concerning C-peptide assay, both in basal and stimulative conditions, in insulindependent long-and short-term diabetes. In 1 case of organic, and 2 cases of functional hyperinsulinism, the test gave useful clinical information. The method of L. Heding-Novo Research Institute, Bagsvaerd, Denmark-, with previous elimination of proinsulin and insulinantibody in patients with high values of IgG insulin binding, proved to be suitable to endocrinological routine.
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PMID:[Determination of plasmatic C-peptide and its clinical uses]. 39 64

Development of diabetes mellitus is a common complication of side to side porta-caval anastomosis (PCA). Five patients with liver cirrhosis and portal hypertension have been studied with intravehous (IVGTT, 0,5 g/Kg B.W.) and oral (OGTT, 1 g/Kg B.W.) glucose tolerance tests before and three weeks after PCA. Fasting plasma glucose was 84 +/- 7 before and 87 +/- 3 mg/dl after PCA. Fasting IRI increased from 17 +/- 3 to 31 +/- 6 microU/ml. The pattern of plasma glucose and IRI response to IVGTT did not change after PCA. Plasma glucose resonse to OGTT after PCA showed only an earlier rise at 60 instead of 90 minutes, whereas IRI resonse (area under the insulin curve) was significantly enhanced (from 12.4 to 19.8 U/l, p < 0.05). These data suggest a role of gut polipeptides in determining hyperinsulinemia and insulin resistence in PCA patients.
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PMID:[Glucose tolerance and insulinemia in patients with hepatic cirrhosis and portal hypertension treated by portacaval anastomosis]. 39 34

A case of a 19-year-old, non-obese female with insulin resistant diabetes mellitus and polycystic ovary syndrome was reported. The maximal insulin requirement attained 360 units per day, but a satisfactory control of diabetes did not follow. The patient's serum contained not only anti-insulin antibodies, but also possible anti-insulin receptor antibodies which were demonstrated by the 125I-insulin binding test using insulin receptors derived from human placental plasma membrane. The insulin resistance in this case was assumed to be caused primarily by possible blocking antibodies to insulin receptors and partly by anti-insulin antibodies because of the following observations. First, high serum free insulin (165 microunits/ml) without hypoglycemia indicates the presence of insulin resistance due to other factors than antiinsulin antibodies. Second, the titer of 125I-insulin binding capacity of serum was not unusually higher than those seen in chronically insulin-treated diabetics. Third, immunologically heterospecies insulin (fish insulin) was also ineffective. The clinical features such as absence of ketoacidosis and association with polycystic ovary syndrome resemble those of an unique diabetic syndrome reported previously though acanthosis nigricans and endogenous hyperinsulinemia were not found in this case. Her insulin resistance remitted spontaneously and over the next 18 months' observation, her diabetes remained regulated without insulin therapy.
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PMID:A case of insulin resistant diabetes with possible antibodies to insulin receptors. 43 98

We studied the effects of short-term (5 days) and long-term (2 wk) high carbohydrate (75%) feedings on insulin binding to isolated adipocytes and insulin sensitivity in vivo in normal subjects. Ingestion of the high carbohydrate diet led to daylong hyperinsulinemia in both short- and long-term groups. Insulin binding to isolated adipocytes was decreased in both groups; in the short-term groups this decrease in insulin binding was caused by a decrease in the receptor affinity, whereas in the long-term group it was caused by a decrease in receptor number. On the other hand, despite this decrease in insulin binding, total in vivo insulin sensitivity was markedly improved in both groups. In conclusion, (1) the short-term adaptive response of the insulin receptor is a decrease in binding affinity whereas the long-term response is a decrease in receptor number, (2) sustained and chronic hyperinsulinemia can lead to a decrease in the number of cellular insulin receptors, (3) high carbohydrate diets lead to a general increase in insulin's ability to promote glucose removal from plasma, and (4) the paradox of enhanced insulin sensitivity in the face of decreased insulin binding can be explained if high carbohydrate diets also lead to an increase in the activity of steps in glucose metabolism distal to the insulin receptor.
Diabetes 1979 Aug
PMID:Effect of a high carbohydrate diet on insulin binding to adipocytes and on insulin action in vivo in man. 44 30

The response of gastric inhibitory polypeptide (GIP) levels to oral glucose in 11 insulin-dependent diabetics was compared to that in 8 age- and sex-matched healthy controls to determine whether they would show the pattern of GIP hypersecretion reported by other workers in maturity-onset, insulin-independent diabetes. One gram of glucose per kg bw resulted in a higher level of glycemia and a significantly diminished GIP response in diabetics when compared to controls (6,018 +/- 1,337 vs. 11,343 +/- 2,353 pg/ml.180 min min, respectively). There was virtually no beta cell response in the diabetics, as measured by changes in the levels of free insulin and connecting peptide. A significant lowering of glucagon levels occurred in the controls, while an inconsistent response was seen in the diabetics. An insulin infusion test was administered to test the hypothesis that insulin suppresses GIP secretion. Although hyperinsulinism, hypoglycemia, and suppression of endogenous insulin secretion were produced in the controls, no suppression of baseline GIP was detected. Similarly, hyperinsulinism and hypoglycemia failed to suppress baseline GIP levels in the diabetics. These results do not support a direct role for insulin in suppressing GIP in normal or diabetic subjects.
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PMID:Gastric inhibitory polypeptide response to hyper- and hypoglycemia in insulin-dependent diabetics. 45 45


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