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

Insulin resistance, which may precede the development of non-insulin-dependent diabetes mellitus in Pima Indians, appears to result from a postreceptor defect in signal transduction in skeletal muscle. To identify the putative postreceptor lesion responsible for insulin resistance in Pima Indians, we investigated the influence of insulin on the activity of casein kinase II (CKII) in skeletal muscle of seven insulin-sensitive, four insulin-resistant, nondiabetic, and five insulin-resistant diabetic Pima Indians during a 2 h hyperinsulinemic, euglycemic clamp. In sensitive subjects, CKII was transiently activated reaching a maximum over basal activity (42%) at 45 min before declining. CKII was also stimulated in resistant (19%) and diabetic (34%) subjects. Basal CKII activity in resistant subjects was 40% higher than in either sensitive or diabetic subjects, although the concentration of CKII protein, as determined by Western blotting, was equal among the three groups. Basal CKII activity was correlated with fasting plasma insulin concentrations, suggesting that the higher activity in resistant subjects resulted from insulin action. Extracts of muscle obtained from all three groups either before or after insulin administration were treated with immobilized alkaline phosphatase, which reduced and equalized CKII activity. These results suggest that insulin stimulates CKII activity in human skeletal muscle by a mechanism involving phosphorylation of either CKII or of an effector molecule, and support the idea that elevated basal activity in resistant subjects results from insulin action. It appears that the ability of insulin to activate CKII in skeletal muscle is not impaired in insulin-resistant Pima Indians, and that the biochemical lesion responsible for insulin resistance occurs either downstream from CKII or in a different pathway of insulin action.
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PMID:Activation of skeletal muscle casein kinase II by insulin is not diminished in subjects with insulin resistance. 199 82

The mean values of body mass index, haemoglobin A1, serum protein, total lipids, triglycerides, lactate dehydrogenase, alkaline phosphatase, amylase and beta-glucuronidase and heart rate and blood pressure and blood urea levels of Libyan diabetic patients with secondary complications are significantly higher than those of the patients without secondary complications. However, the mean values of fasting blood glucose, serum cholesterol and beta-N-acetylglucosaminidase of patients without complications are higher than those of the patients with secondary complications. The duration of diabetes in patients with secondary complications was 10.2 +/- 1 years while that of patients without complications was 5.2 +/- 0.65 years. The significance of these results is discussed.
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PMID:Secondary diabetic complications and biochemical parameters. 209 82

We determined neutrophil alkaline phosphatase (NAP) activity in diabetic patients in conjunction with HbA1c levels. NAP was estimated using semiquantitative cytochemical technique, and we studied its activity in different groups of diabetic patients. We found that NAP score is correlated with the HbA1c level. Non-diabetic patients were used as controls, in whom NAP score and HbA1c were found normal. In diabetic patients the NAP activity and the HbA1c level were altered similarly during the various phases of the disease. Our findings indicate that NAP score could be used as a simple new parameter for diabetes. The pathophysiologic mechanism of our observations needs further investigation.
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PMID:Association of neutrophil alkaline phosphatase activity and glycosylated haemoglobin in diabetes mellitus. 210 65

In an ongoing study of brain microvasculature in humans at autopsy, we had the opportunity to analyze the overall scheme of this vascular supply. The native endothelial membrane enzyme, alkaline phosphatase, is used to precipitate black lead sulfide salt in the vessel wall, rendering the brain microvasculature visible by both light microscopy and microradiography. There are six distinct patterns of intraparenchymal afferent blood supply to the supratentorial brain: short arterioles from a single source (e.g., those in the cortex); short- to intermediate-length arterioles, single source (anterior two-thirds of the corpus callosum); short- to intermediate length arterioles and arteries, dual source (subcortical U fibers); intermediate-length arterioles and arteries, triple source (extreme/external capsule and claustrum); long arteries and arterioles, single source (centrum semiovale); and large, long muscular arteries, single source (thalamus and basal ganglia). The nature of this arrangement offers some protection to certain regions of the cerebrum from circulatory challenges such as hypotension, while leaving other areas vulnerable. The distal arterioles supplying two of these protected regions, the U-fiber area and the extreme/external capsule and claustrum area, also exhibit the feature of interdigitation, which can offer additional collateral potential from one arteriolar territory to the next. Aging, hypertension, diabetes mellitus, and atherosclerosis can have a significant impact on brain microcirculation. The way in which vascular patterns dictate the distribution of these effects is discussed. The ability to stain the cerebral microvessels and demonstrate the finer points of their patterns in sections and microradiographs has enabled us to resolve some long-standing questions about vascular connections and directions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Features of the cerebral vascular pattern that predict vulnerability to perfusion or oxygenation deficiency: an anatomic study. 211 4

Hyperparathyroid bone disease is a common complication of end stage renal failure, particularly in patients on maintenance haemodialysis. Several studies have, however, shown a near absence of hyperparathyroid bone disease in diabetic patients who have been receiving haemodialysis for periods of up to 4 years. We have studied biochemical indices of mineral metabolism in 54 consecutive pre-dialysis patients with moderate to severe renal impairment. Deteriorating renal function was associated with developing hypocalcaemia and hyperphosphataemia. Hypocalcaemia was strongly related to increased severe alkaline phosphatase activity (p less than 0.001), suggesting the development of hyperparathyroidism. Five patients with hypocalcaemia and increased alkaline phosphatase were studied in detail. All had elevated serum concentrations of parathyroid hormone and histological signs of hyperparathyroidism on bone biopsy. Three of the patients had low serum 25 hydroxyvitamin D levels with associated osteomalacia, the other 2 patients were notable for their long duration of renal failure. In the long-term (greater than 4 years) we also observed the development of hyperparathyroidism in a small group of diabetic patients maintained on haemodialysis. We conclude that diabetic patients are not uniquely protected against renal osteodystrophy. Although the prevalence of hyperparathyroidism may be lower in diabetic patients than in those with other types of renal disease, the same factors which predispose to bone disease in non-diabetic patients (long duration of renal failure, low serum 25 hydroxyvitamin D and long periods on haemodialysis) also operate in the diabetic population.
Diabetes Res 1990 Aug
PMID:Hyperparathyroid bone disease in diabetic renal failure. 213 93

The basic prerequisite of treatment of diabetic osteopenias is perfect metabolic compensation of diabetes. Insulin administration is an advantage in this respect, as it enhances calcium absorption from the gut and reduces its urinary excretion. Conversely, oral antidiabetics interfere in a negative way with vitamin D metabolism and thus also calcium metabolism and mineralization of bone. The combination of calcium, small doses of vitamin D, NaF and exercise used in the treatment of diabetic osteoporoses leads in general to a significant rise of the calcium serum level, an insignificant rise of the phosphorus level and it reduces alkaline phosphatase activity. A certain disadvantage is the elevated urinary calcium excretion. The main drug in diabetic osteomalacia are usually large doses of vitamin D. The rise of the serum calcium level improves the metabolic compensation of diabetes in a linear fashion. Thiazide diuretics used to reduce excessive calciuria cause slight deterioration of the glucose tolerance but the compensation does not cause major difficulties.
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PMID:[Diabetic osteopathies. 6. Treatment and its pitfalls]. 213 68

Between Nov. 1981 and Nov. 1987 103 patients preselected for chemotherapy combined with surgery, therefore with local extension within homolateral mediastinal lymph nodes, with no signs of remote metastases, PS greater than or equal to 70, with no contraindication for resectional surgery including pneumonectomy, no diabetes, no prior treatment underwent first staging. Staging included: case history, physical examination, full blood count, biochemical tests (alkaline phosphatase, SGOT, GGTP, LDH), CEA, X-ray assessment including CT scan of the chest, bronchoscopy, peritoneoscopy, liver scan (US was not routinely used at the beginning), bilateral bone marrow trephine biopsy, and bone scan. Staging was discontinued when secondaries were detected in one, the more so as in two organs or systems (25 pts), and/or bronchoscopic contraindication for thoracotomy (11 pts), and this group of patients was out of the study. To 67 patients chemotherapy was given and after 3 courses these patients were reevaluated. In 21 patients PD, NC or CR was found. Forty six patients with PR underwent supplementary staging procedures: CT of the brain, CT of the upper retroperitoneal space and liver. Metastatic sites were found in 7 patients. Limited disease was identified in 39 patients. Limited-stage disease can be determined only after exclusion of extensive disease on the ground of: case history, physical assessment, X-ray of the chest (PA + lateral) + CT chest scan, bronchoscopy with biopsy or cytology, and outside the chest: 1. bone marrow trephbine biopsy and bone scan--bone marrow and skeleton, 2. CT head scan--brain, 3. CT abdominal scan--upper retroperitoneal space and liver.
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PMID:[Identification of a limited form of small cell lung cancer among 103 patients pre-selected for chemotherapy combined with surgery]. 217 35

1. We determined the organ of origin and possible mechanism of translocation into the circulation of alkaline phosphatase (ALPase) in the diabetic rat. 2. Experimental diabetes was induced by injection of streptozotocin, resulting in a 8.2-fold elevation in serum ALPase activity. In this case, the major ALPase isozyme detected in serum was intestinal ALPase. 3. In in vitro experimental systems, ALPase was readily released from the duodenal plasma membrane by bacterial phosphatidylinositol-specific-phospholipase C (PI-PLase C) but little if any was released from the ileal membrane. 4. Serum and ileal ALPases were identical in terms of molecular size, whereas duodenal ALPase clearly differed from the serum enzyme. 5. Based on an investigation of the sugar moiety, more of the fraction having higher concanavalin A affinity was found in serum ALPase than with in the case of either of the intestinal ALPases. Serum and intestinal ALPases also differed slightly regarding isoelectric points. 6. Consequently, these data suggest that the serum ALPase of the diabetic rat is derived from ileal ALPase, and it is unlikely that the appearance of ALPase in the circulation is simply the result of solubilization by the action of PI-PLase C or phospholipase D.
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PMID:Translocation of intestinal alkaline phosphatase in streptozotocin-induced diabetic rats. 225 56

The purpose of our study was to determine if streptozotocin induced diabetes (SID) in rats produces alterations in hepatic function, as described in poorly controlled diabetic patients, and if islet transplantation (islet-Tx) would subsequently ameliorate this status. Hepatocellular dysfunction was evaluated by the aspartate aminotransferase (SGOT) and the alanine aminotransferase (SGPT) activities in plasma. For the evaluation of cholestasis the plasma alkaline phosphatase (APase) activity was used. These determinations were performed in normal, SID, SID with Islet-Tx, and SID Wistar rats with sham-Tx. Also, glucose was measured in plasma samples, as well as histological studies of the liver were performed. More than 1,000 isogeneic islets (islet-Tx group) or non viable insular tissue (sham-Tx group) were transplanted via mesenteric ileal vein three weeks after SID. The results showed that SID in rats produces alterations in the hepatic function as well as in the structure of the hepatocytes, and the normalization of carbohydrate metabolism by islet transplantation restores normal hepatic function and morphology.
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PMID:Normalization of the altered liver function tests after islet transplantation in diabetic rats. 226 34

A newly recognized disease in dogs, ulcerative dermatosis associated with diabetes mellitus (diabetic dermatopathy), was diagnosed in 2 dogs with pancreatic endocrine tumors that had immunohistologic evidence of glucagon production. Dogs developed diabetes mellitus in the later stages of the illness, months after the skin disease was first observed. Liver disease was identified and characterized by high serum alkaline phosphatase and alanine transaminase activities. Clinically, erythema and crusting involved the footpads, the face, perioral and genital skin, and ventrum. Histologically, skin lesions were intercellular and intracellular edema and necrosis of the upper half of the epidermis and diffuse parakeratosis. Clinically and histologically, skin lesions closely resembled necrolytic migratory erythema of people, a skin disease that usually is associated with a glucagon-secreting pancreatic endocrine tumor and diabetes mellitus (glucagonoma syndrome): The morphologically descriptive term, superficial necrolytic dermatitis, was preferred over the previously proposed names hepatocutaneous syndrome and diabetic dermatopathy, which each connote only a single feature of the disease.
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PMID:Glucagon-producing pancreatic endocrine tumors in two dogs with superficial necrolytic dermatitis. 227 59


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