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

Prostaglandin E(2) (PGE(2)) infusion in normal humans inhibited acute insulin responses to a glucose (5 g i.v.) pulse (response before PGE(2) = 593 +/- 104%; during PGE(2) = 312+/-55%; mean+/-SE, mean change 3-5 min insulin,% basal, P < 0.005). This effect was associated with a decrease in glucose disappearance rates (K(G) before PGE(2) = 0.73+/-0.07; during PGE(2) = 0.49+/-0.06%/min, P < 0.025). Acute insulin responses to arginine (2 g i.v.) were not affected by PGE(2) (response before PGE(2) = 592+/-164%; during PGE(2) = 590+/-118%; P = NS). Infusion of sodium salicylate (SS), an inhibitor of endogenous prostaglandin synthesis, augmented acute insulin responses to glucose in normals (response before SS = 313+/-62%; during SS = 660+/-86%; P < 0.001). In adult-onset diabetes with fasting hyperglycemia, SS restored absent acute insulin responses to glucose (20 g i.v.) pulses (response before SS = 5+/-6%; during SS = 97+/-24%; P < 0.005). This was accompanied by a fourfold augmentation in second phase insulin secretion (second phase before SS = 1,696+/-430%; during SS = 5,176+/-682%; change 10-60 min insulin, muU/ml.min,% basal, P < 0.001) and by acceleration of glucose disappearance rates (K(G) before SS = 0.56+/-0.06; during SS = 1.02+/-0.17%/min, P < 0.005). These findings uniquely demonstrate that (a) PGE(2) inhibits glucose-induced acute insulin responses and decreases glucose disposal in nondiabetic humans and (b) SS restores acute insulin responses, augments second phase insulin secretion, and accelerates glucose disposal in hyperglycemic, adultonset diabetics. It is hypothesized that endogenous PGE synthesis may play a role in defective insulin secretion and glucose intolerance in diabetes mellitus.
J Clin Invest 1977 Sep
PMID:A role for prostaglandin E in defective insulin secretion and carbohydrate intolerance in diabetes mellitus. 33 May 66

The effect, if any, of diabetes mellitus on the fetal renal tubule has not been previously studied. The concentration of beta2 microglobulin in amniotic fluid is a marker of fetal renal tubular function and normally decreases with advancing gestation, implying increasing tubular function. This relationship was found to be disrupted in 12 diabetic pregnancies, suggesting that the fetal renal tubular cell may represent an example of altered fetal functional maturation occurring during diabetic pregnancy.
Am J Obstet Gynecol 1977 Sep 15
PMID:Fetal renal tubular function during late pregnancy and diabetes mellitus. 33 54

Thirty-nine patients (14 non-diabetics, 8 chemical diabetics, and 17 overt diabetics) with circulating islet cell antibodies (ICA) were studied. Insulin and glucagon secretion after oral (100 g) and intravenous glucose loading (200 mg/kg bolus injection followed by an infusion of 20 mg/min over 60 min) and arginine infusion (25 g over 30 minutes) were evaluated in these patients and in non diabetic and diabetic ICA-negative controls. In the non-diabetic groups with or without ICA, insulin and glucagon responses to glucose were similar. Moreover, in ICA positive patients the response of these hormones to arginine infusion was reduced. Similar alterations in insulin and glucagon secretion were observed in the CIA positive and negative patients with chemical or overt diabetes. In particular, fasting hyperglucagonaemia and glucagon hyperresponse to arginine are associated with a lack of insulin secretion in the patients with overt diabetes. Hormonal differences between diabetics with and without ICA could not be detected.
Diabetologia 1977 Sep
PMID:Insulin and glucagon secretion in diabetic and non-diabetic patients with circulating islet cell antibodies. 33 69

Twenty-eight cases of peritoneal infections occurring in 686 transplant patients (4%) are reported. The mortality was 78.5% (22 of 28 patients) and accounted for 13.2% of all transplant deaths. Recipients of cadaver kidneys were more prone to develop intraperitoneal infection, whereas the age, the presence of diabetes, and the tissue typing had no influence on the likelihood to develop intraperitoneal infections. Sixteen patients developed intraperitoneal infection secondary to the transplantation or another operation, whereas the intraperitoneal infection was due to a disease process unrelated to previous surgery in 12 patients. Only 64% of the patients presented with abdominal symptoms, 24 presented with septic shock, and 11 with a wound infection without peritoneal signs. The uncharacteristic clinical findings resulted in a delay of 8.7 days between the onset of symptoms and the recognition of the peritoneal infection and made a preoperative diagnosis possible in only 22 patients. It became clear that patients with generalized peritonitis, concomitant distant infections, opportunistics organisms in the peritoneal cavity, and the infections caused by postoperative complications have a poorer prognosis than the remainder of the group. Early recognition of the problem, especially after operation, and vigorous treatment seem to be the keys for improved results in the treatment of this serious condition.
Surgery 1978 Sep
PMID:Prognostic factors of peritoneal infections in transplant patients. 35 17

Progress in our understanding diabetic angiopathy has been slow, but we are now learning a number of lessons of interest to the cardiologist. Diabetic angiopathy is a collective term for conditions specific to the diabetic state and related to its duration more than to patient age. The angiopathy produces calcification of the media of larger arteries, but its major effects are in the microcirculation. Intense interest in one feature, skeletal muscle capillary basement membrane thickening, has dominated the last decade. Capillary basement membrane thickening, while characteristic of diabetes, is associated with little direct impairment of the microcirculatin. It appears to play no role in the pathogenesis of diabetes itself. The pathology of diabetic retinopathy and diabetic nephropathy suggests that arteriolar changes may be the major mediator of diabetic angiopathy. This concept is supported by the interactions between hypertension and diabetes in the eye and kidney. The course of diabetes of youthful onset differs from that of maturity onset. The relative frequency of diabetic angiopathy is higher, and of atherosclerotic complications is lower. This has made it difficult to demonstrate the potential value of preventive measures. Benefit to one type of problem may become hidden by worsening of the other. If the diabetic benefits from what is learned about how ischemic heart disease risk can be reduced, he will require even more effective management to prevent or control diabetic angiopathy.
Am Heart J 1978 Sep
PMID:Diabetic angiopathy--its lessons in vascular physiology. 35 70

In order to investigate whether patients with long-standing juvenile diabetes mellitus (onset of diabetes before the age of 30) and a low daily insulin requirement (less than 0.50 units/kg body weight) still have functioning B-cells, plasma C-peptide was determined after stimulation (OGTT and glucagon/tolbutamide) in 64 patients with diabetes of more than 18 years' duration (mean 31 years). Measurable endogenous insulin production was found in 24% of the patients. The prevalence of severe retinopathy was lower in the secretors than in the non-secretor group. There was no difference in insulin antibody concentration between the two groups. Furthermore, the insulin requirement in the secretor group was relatively constant during the course of diabetes. Metabolic control was similar in both groups. It is concluded that a persisting but low activity of endogenous insulin production can be found in many long-term juvenile diabetics with a low insulin requirement, while others without any residual beta-cell function develop a low insulin requirement for unknown reasons.
Diabetologia 1978 Sep
PMID:Persistent insulin secretion, assessed by plasma C-peptide estimation in long-term juvenile diabetics with a low insulin requirement. 35 94

In all diabetic animal models studied to date, microangiopathic complications develop which can be prevented by tight control and reversed by either islet cell transplantation or transplanting the diabetic kidney into a nondiabetic environment. In humans the prevalence of these complications in secondary diabetes mellitus is similar to the prevalence in genetic diabetes. Furthermore, mesangial basement membrane thickness is normal at the onset of the disease and increases shortly thereafter. These two facts strongly suggest that the microangiopathic complications are not an independent genetic component but rather are secondary to the metabolic derangements of uncontrolled diabetes. Normal kidneys transplanted into diabetic recipients developed the vascular lesions of diabetes. Conversely, two diabetic kidneys inadvertently transplanted into nondiabetic recipients showed clearing of the vascular lesions.Most retrospective studies support the conclusion that control is associated with lessened complications. The three prospective studies published to date also support this hypothesis. Because glucose concentrations cannot be brought to normal levels by present methods, the critical question is whether a major emphasis on restoring metabolism to as nearly normal as possible will help ameliorate the microangiopathic complications in our patients. The accumulated evidence would strongly favor an affirmative answer. Two daily injections of intermediate-acting insulin supplemented with small amounts of short-acting insulin as needed is one method to approach this goal.
West J Med 1978 Sep
PMID:The case for control in diabetes mellitus. 36 Jun 22


Diabetes 1979 Sep
PMID:Venezuelan encephalitis virus-induced alterations in carbohydrate metabolism in geneticaly diabetic mice. 38 Oct 78


Diabetes 1979 Sep
PMID:Necrology: Francis D.W. Lukens, M.D. 38 Oct 79

To clarify further the etiology of the carbohydrate intolerance in idiopathic hemochromatosis, we investigated the glucose, insulin, C-peptide, and glucagon responses to arginine (0.5 g/kg) infused during 30 min in lean normal subjects; in insulin-requiring subjects with hemochromatosis, genetic diabetes, and total pancreatectomy; and in nondiabetic cirrhotic subjects without portosystemic shunting. Serum insulin, C-peptide, and glucagon responses (30K antibody) were determined by RIA, and glucose level was determined by a glucose oxidase technique. Hemochromatotic and genetic diabetic subjects had similar basal glucose (157 +/- 25 vs. 168 +/- 40 mg/dl) and C-peptide (0.73 +/- 0.42 vs. 0.65 +/- 0.22 ng/ml) values, with subnormal C-peptide peak responses to stimulation (1.05 +/- 0.38 and 1.40 +/- 0.83 vs. 3.95 +/- 0.4 ng/ml in normals; P less than 0.05). No glucagon or C-peptide response to arginine was seen in any pancreatectomized subject. Similar but excessive glucagon levels were present in hemochromatosis, diabetes, and cirrhosis under basal conditions (166 +/- 24, 232 +/- 111, and 263 +/- 116 vs. 76 +/- 15 pg/ml; P less than 0.05) and after arginine stimulation (782 +/- 80, 834 +/- 123, and 902 +/- 275 vs. 489 +/- 81 pg/ml; P less than 0.05) when compared with normals. The excessive glucagon levels found in hemochromatosis, diabetes mellitus, and cirrhosis contrast to the absent response in pancreatectomized subjects and indicate that generalized islet cell destruction is not the major factor in diabetic hemochromatotic subjects.
J Clin Endocrinol Metab 1979 Sep
PMID:Pancreatic alpha-cell function in diabetic hemochromatotic subjects. 38 22


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