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

A diminution of the cross sectional area of myelinated fibres in the common peroneal nerve was observed in rats four weeks after the induction of diabetes with streptozotocin. Small fibres were affected more than larger ones and the axon reduction was twice that of the myelin sheath. The fibre diminution and the decreased axon/myelin ratio may explain the slowing of nerve conduction in experimental diabetes.
Diabetologia 1976 Dec
PMID:Axonal dwindling in early experimental diabetes. I. A study of cross sectioned nerves. 13 57

In a morphometric study of isolated fibres of the common peroneal nerve in short-term diabetic rats reduced fibre calibre was observed. No segmental demyelination or remyelination was found, but the nodes of Ranvier were slightly widened and paronodal bulbi were swollen relative to fibre calibre. It is suggested that axonal dwindling is the primary event in experimental diabetes. The reduction of the myelin sheath may be a consequence of the abnormal nerve cell offshoot. The results obtained suggest that streptozotocin diabetes in the rat is a useful model for the elucidation of diabetic neuropathy.
Diabetologia 1976 Dec
PMID:Axonal dwindling in early experimental diabetes. II. A study of isolated nerve fibres. 13 58

1. Kidney weight and content of protein, RNA and DNA were measured in rats with streptozotocin diabetes of varying duration. 2. Diabetic rats had larger kidneys than control rats: after 3 days of diabetes the weight increase was 15 per cent and after 42 days of diabetes it was 90 per cent. The protein content rose in parallel to the weight. 3 RNA content was already increased after 36 h of glycosuria, whereas DNA content was unchanged for the first 3 days of diabetes, and increased thereafter. The protein/DNA ratio increased rapidly during the first 3 days but remained constant thereafter. 4. Insulin treatment decreased the renal weight gain by about 67 per cent during the first 8 days of diabetes, but did not prevent the increase in DNA. When insulin was started after 25 days of diabetes there was only a slight regression of kidney growth.
Clin Sci Mol Med 1976 Dec
PMID:Renal hypertrophy in streptozotocin-diabetic rats. 13 97

D-glucose in the pyranose (ring) form exists as two anomers. The alpha-anomer is more effective than the beta-anomer in promoting insulin secretion, suppressing that of glucagon, and protecting beta-cells against alloxan toxicity. Streptozotocin (SZ), a beta cell toxin, is composed of a cytotoxic moiety, 1-methyl 1-nitrosourea, attached to carbon-2 of glucose and exists as either of two anomers in the pyranose form. In 24-hour-fasted male rats, predominantly alpha- or predominantly beta-SZ was injected intravenously and plasma glucose levels were obtained 48 hours later. The alpha-anomer produced significantly greater beta-cell necrosis at doses of 30, 35, and 40 mg./kg. body weight. At higher doses, no differences between the alpha and beta anomers were observed. 3-O-Methyl glucose (3-OMG) protected against both SZ anomers; however, the alpha-SZ remained more toxic. Larger doses of glucose protected against the lower doses of SZ and, under such conditions, the individual glucose anomers appeared equally potent. Finally, mannitol at comparable molar concentrations was ineffective in protecting against the SZ toxicity. This study suggests that streptozotocin's beta cell toxicity is mediated through recognition by the beta cell. In addition, 3-OMG and, to a lesser but significant extent, glucose were shown to protect against the streptozotocin toxicity, whereas mannitol did not.
Diabetes 1977 Dec
PMID:Pancreatic beta cell toxicity by streptozotocin anomers. 14 86

Plasma androgen levels were determined in women assigned to the following groups: idiopathically hirsute, diabetic, both idiopathically hirsute and diabetic, and normal. The androgens examined were androstenedione (AD), dihydrotestosterone (DHT), testosterone (T), and dehydroepiandrosterone (DHEA). We find statistical differences between young (less than 38 years) and older (larger than or equal to 38 years) controls at confidence levels of p less than or equal to 0.01 for AD, DHT, and T and of p less than or equal to 0.05 for DHEA. The results indicate that peak circulating androgen levels occur prior to age 30-35 years for women. There are no significant differences between the young controls and young idiopathically hirsute subjects, but a statistical difference exists between older hirsute and older controls for all four androgens (p less than or equal to 0.05). When a comparison is made among the diabetic, hirsute diabetic, and older control groups (all groups larger than or equal to 38 years), the diabetic group is significantly higher than the control in plasma AD (p less than or equal to 0.01) and DHEA (p less than or equal to 0.05). These same two steroids are also higher in the diabetic group than in the hirsute diabetic group (p less than or equal to 0.05), while the latter differs from controls only in testosterone levels (p less than or equal to 0.05). DHT levels are similar for all three groups.
Diabetes 1977 Dec
PMID:Plasma androgen concentrations in diabetic women. 14 87

Forty-six separate renal tumours developed in 36/80 Wistar male rats given a single i.v. dose of streptozotocin (25 mg/kg body wt) to induce diabetes mellitus. Fourteen of the tumours were epithelial in type, 8 were wholly mesenchymal and 24 were largely mesenchymal but also contained epithelial elements. The purely epithelial tumours correspond to the renal adenomas and adenocarcinomas seen in man. The mesenchymal tumours were composed either of undifferentiated spindle cells or of a mixutre of poorly differentiated mesenchyme and epithelial glands. Microscopically, the mixed tumours resembled the nephroblastomas seen in man; both elements appeared to be malignant, but in the absence of metastases this remains unproven. The management of the diabetic state did not influence the incidence of tumours, but insulin appeared to enhance tumour growth.
Br J Cancer 1977 Dec
PMID:Streptozotocin-induced renal tumours in rats. 14 71

1. Injection of L-tryptophan (750 mg/kg body wt.) led to pronounced hypoglycaemia in fed and 48 h-starved rats. 2. The hypoglycaemic effect is blocked by pretreament with p-chlorophenylalanine, compound MK-486 [Carbidopa: L-alpha-(3,4-dihydroxybenzyl)-alpha-hydrazinopropionic acid monohydrate] or methysergide, and potentiated by pargyline. 3. 5-Hydroxy-L-tryptophan is more potent and induces a more rapid hypoglycaemia than does tryptophan. Other tryptophan metabolites were not associated with hypoglycaemia. 4. Adrenalectomy increases, and acute experimental diabetes strongly decreases, the sensitivity of rats to tryptophan induction of hypoglycaemia. Diabetic animals were also insensitive to 5-hydroxytryptophan. 5. Metabolite concentration changes in the livers from tryptophan-treated 48h-starved and diabetic animals were consistent with a rapid inhibition of gluconeogenesis. This did not correlate with the hypoglycaemic response. 6. Tryptophan treatment was associated with a significant increase in the plasma [beta-hydroxybutyrate]/[acetoacetate] ratio; there were no changes in the plasma concentrations of urea, triacyglycerol, non-esterified fatty acids and glycerol. 7. These observations suggest that the hypoglycaemic action of tryptophan is mediated through formation of intracellular 5-hydroxytryptamine, and is unrelated to the inhibition of gluconeogenesis. It is unlikely that this increased synthesis of 5-hydroxytryptamine involves directly either the adrenal glands or the central nervous system.
Biochem J 1977 Dec 15
PMID:Tryptophan and the control of plasma glucose concentrations in the rat. 14 76


Diabetes 1978 Dec
PMID:Hemoglobin AIc in the glucose-intolerant, streptozotocin-treated or pancreatectomized macaque monkey. 15 23

The records of 281 patients undergoing aortic grafting to 522 femoral arteries over a period of 18 years were reviewed. Fifty-four patients suffering graft limb occlusion to 71 femoral arteries requiring subsequent secondary repair were identified for detailed analysis. Occlusive disease of the profunda femoris artery was identified as the primary cause of thrombosis. Repair consisted of profunda femoris angioplasty, and transfemoral retrograde graft thrombectomy was possible in all but three instances which were managed by cross-over femoral-femoral bypass. In no instance was laparotomy and abdominal graft replacement necessary. The 30 day operative survival and graft patency were 100%. Analysis of factors that have influenced late graft patency demonstrated that the key factors were the method of profundaplasty and the association of diabetes mellitus. When autogenous profundaplasty (on-lay arterial patches, saphenous vein, or limited endarterectomy) was employed, the overall patency combining diabetics and non-diabetics was two and one-half times greater than when profundaplasty was performed with an on-lay Dacron((R)) patch. If diabetics were separated from nondiabetics in the autogenous angioplasty group, the 36 month patency for non-diabetics was 85%, and 0% for diabetics. We conclude that autogenous profundaplasty provides considerable advantage from the standpoint of long-term patency and that the diabetic patients are relatively poor candidates for secondary arterial repair of an occluded aortofemoral bypass graft.
Ann Surg 1978 Dec
PMID:Autogenous profundaplasty: The key to long-term patency in secondary repair of aortofemoral graft occlusion. 15 34

The importance of the hepatic portal circulation in the response to insulin was assessed in streptozotocin-diabetic rats transplanted with syngeneic fetal pancreases. Partial reversal of diabetes was accomplished by transplantation of two or three fetal pancreases beneath the capsule of the kidney; complete reversal followed shunting of the venous drainage from the transplants to the liver. Plasma glucose after streptozotocin of 509+/-31 mg/dl (mean+/-SEM) fell after transplantation to 395+/-23 and after the shunt to 143+/-5 mg/dl. Urine volume fell from 84+/-4 to 50+/-5 ml/d and then to normal (17+/-1 ml/d) after the shunt. Glucose excretion which was 8.1+/-0.3 g/d after streptozotocin fell after transplantation to 4.8+/-0.3 g/d and after the shunt completely disappeared from the urine. The disappearance rate of glucose injected into the circulation, which was 0.50+/-0.07%/min in untreated diabetes, increased to 1.39+/-0.38%/min after transplantation and to 2.52+/-0.31%/min after the shunt, not different from normal controls (2.79+/-0.25). Plasma immunoreactive insulin (IRI) was below normal (25-35 muU/ml) and unresponsive to glucose in untreated diabetic rats. After transplantation IRI levels ranged from 73-223 muU/ml and there was no rise after glucose injection. After the shunt both the basal IRI (36+/-5 muU/ml) and the peak response to glucose at 10 min (58+/-7 muU/ml) were the same as in normal controls (42+/-4 and 62+/-7 muU/ml, respectively). The fall in IRI after the shunt is explained by increased extraction of insulin passing into the liver and also diminished secretion. After removal of the transplants plasma glucose and urine values returned almost to pretransplant levels. Secretion of insulin by transplanted pancreases into the liver enhances the effectiveness probably by increased extraction and action and reveals the importance of the normal route for insulin delivery.
J Clin Invest 1979 Dec
PMID:Importance of hepatic portal circulation for insulin action in streptozotocin-diabetic rats transplanted with fetal pancreases. 15 16


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