Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the effect of streptozotocin induced diabetes on glomerular basement membrane (GBM) synthesis, an isolated rat glomerular preparation has been developed, and its metabolic properties have been defined. The chemical composition of normal rat GBM isolated from this preparation closely resembles human GBM. Incubation with [U-14C] lysine leads to prompt incorporation of label into GBM and the subsequent appearance of labeled hydroxylysine. A 1-h lag before detection of labeled hydroxylysine in GBM suggests a delay in the release of GBM precursors. Significantly lower counts appeared in the nondialyzable fraction of the medium than in insoluble GBM during pulse-chase experiments, and labeled hydroxylysine accounted for a lower portion of the total counts in the medium (0.85%) than in the GBM (1.98%). Isolated glomeruli were prepared from streptozotocin diabetic rats of 4-6 wks duration. After incubation with [ U-14C] lysine recovery of label in diabetic GBM (88.98+/-8.26 nmol/g GBM) did not differ from age matched controls (82.52 +/- 8.26 nmol/g GBM). In pulse-chase experiments recovery of label in hydroxylysine of diabetic GBM (o.473 +/- 0.082 nmol/g GBM) did not differ from age matched controls (0567+/-0.065 nmol/g GBM). These findings indicate normal rates of GBM synthesis and hydroxylation of lysine residues in animals with streptozotocin diabetes.
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PMID:Glomerular basement membrane: biosynthesis and chemical composition in the streptozotocin diabetic rat. 13 2

1. A polyclonal, monospecific antibody to a constitutive, diabetes-inducible and insulin-reversible cytochrome P-450 isozyme (RLM6) was used to screen a male rat liver cDNA library in lambda gt 11. Six clones harbouring the RLM6 cDNA insert were isolated initially from the expression library and three of these were further plaque-purified and sub-cloned. A 1.1 Kb cDNA insert, representing approximately 65% of the expected full length cDNA was characterized by restriction endonuclease mapping and sequenced by the dideoxy chain-termination method. Comparison of the nucleotide sequence of RLM6 cDNA to that of ethanol-inducible P4502E1 rat cDNA showed the two cDNAs to be identical, the RLM6 cDNA corresponding to nucleotides 310-1402 of the P4502E1 sequence. 2. RLM6 cDNA probe was used in Northern blot and RNA dot blot hybridization analysis to demonstrate that both streptozotocin-induced diabetes and fasting significantly elevated the steady-state level of RLM6 mRNA in male rat liver. Increased RLM6 mRNA level in the diabetic rat resulted in increased RLM6 apoprotein synthesis when polysomal RNA was used in a cell-free, protein-synthesizing system, indicating that the elevated RLM6 level observed in diabetic rats was correlated directly with the increased RLM6 mRNA concentration. 3. Daily insulin treatment of diabetic rats reversed the diabetes-dependent increase in RLM6 mRNA in a time-dependent manner, returning to control values after approximately 2 weeks of continuous insulin treatment. This insulin-dependent decrease of the RLM6 mRNA level was paralleled by a similar time-dependent decrease in serum acetone concentration. 4. Treatment of the male diabetic rat with testosterone also resulted in a decrease in both RLM6 mRNA and in vitro translated apoprotein. 5. Modulation of RLM6 mRNA level in the diabetic rat by insulin and testosterone, and the nucleotide sequence similarity with that of P4502E1 confirms that diabetes-inducible P450RLM6 and ethanol-inducible P4502E1 are coded for by the same gene.
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PMID:Molecular cloning of a cDNA for rat diabetes-inducible cytochrome P450RLM6: hormonal regulation and similarity to the cytochrome P4502E1 gene. 144 86

A 1.5-year-old Saudi girl with hemolytic uremic syndrome is described. She developed hyperglycemia in the acute stage which required insulin therapy. After a short remission, she developed permanent insulin-dependent diabetes mellitus. Review of the literature of the occurrence and the pathophysiology of this phenomenon is presented.
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PMID:Persistent insulin-dependent diabetes mellitus in hemolytic uremic syndrome. 160 86

A 1-page check-off form that can be used to evaluate a woman's risk factors for oral contraceptives, IUD or diaphragm and spermicide, and provide a permanent health record of the evaluation, has been revised to reflect lower-dose pills and new information. Each risk factor is assigned points in columns under each contraceptive method, so that a score of 10 suggests that a contraindication may exist against that method. Some of the changes for orals are lower scores for age 40, unless other risk factors co-exist, especially smoking. Liver disease, hepatitis and gall bladder disease were eliminated, but liver tumors, endometrial cancer and cholestatic jaundice of pregnancy were each given 10 points. Scores were altered slightly for chloasma, hemoglobinopathies, hypertension and diabetes. Scores for the diaphragm were lowered for pelvic relaxation risk but 5 points were introduced for history of urinary tract infection. For IUDs, multiple sexual partners and abnormal bleeding are added as risks.
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PMID:Family-planning risk-scoring system: updated. 201 9

This study tested the hypothesis that the peripheral nerve in the presence of diabetes is more susceptible to chronic nerve compression than it is in the nondiabetic rat. A 1-cm length of sciatic nerve was subjected to chronic compression by banding with a Silastic tube in normal and in streptozotocin-induced diabetic rats. After six months of banding, both the amplitude and conduction velocity of the diabetic banded sciatic nerve were significantly reduced (p less than 0.001) in comparison with the nondiabetic banded rats. These results suggest that in the presence of hyperglycemia, the peripheral nerve is more susceptible to chronic compression.
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PMID:Susceptibility of the diabetic nerve to chronic compression. 335 55

We sought to determine whether differences in the human insulin gene or its immediate flanking sequences could be found in diabetes. Peripheral leukocyte DNA from 217 unrelated persons, including blacks, whites, and Pima Indians, was analyzed by restriction-enzyme digestion, blotting to nitrocellulose filters, and hybridization to cloned [32P]insulin-gene probes. A region of length variation including deletions (0.1 to 0.2 kilobase pairs) or insertions (0.6 to 5.5 kb) of DNA was found only in the immediate 5' flanking region in 33 per cent of the genes examined. A 1.6-kb insertion accounted for 80 per cent of the polymorphism. This variant was found more often in subjects with non-insulin-dependent diabetes than in nondiabetics, regardless of race (P = 0.011). Length polymorphism in the 5' flanking region of the insulin gene may provide a genetic marker for non-insulin-dependent diabetes.
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PMID:Polymorphism in the 5' flanking region of the human insulin gene: a genetic marker for non-insulin-dependent diabetes. 629 21

Beta-2 microglobulin (beta 2 M) is a low molecular weight protein filtered by the renal glomerulus, then reabsorbed and metabolized at the proximal tubule. Its blood concentration is a good renal index, as it is independent from muscle mass and diet contrary to creatinine. We assayed serum beta 2 M in 190 cases of diabetes mellitus divided into 71 non-insulin-dependent and 119 insulin-dependent forms. We found no significant difference between both groups. Serum beta 2 M was not correlated with Hb A 1 C. Conversely, a highly significant positive correlation between beta 2 M and serum creatinine and a negative correlation between beta 2 M and creatinine clearance were demonstrated. Furthermore, patients with borderline serum creatinine and those with normal renal function show very significant differences in mean serum beta 2 M concentrations, thus making combined assay of both parameters advisable. On the other hand, we were unable to evaluate modifications in beta 2 M according to other complications of diabetes mellitus as vascular and neurologic involvement are very often associated with renal dysfunction.
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PMID:[Beta 2 microglobulin in diabetic patients. Apropos of 190 subjects]. 632 52

To study the importance of the residual insulin secretion for the degree of diabetic control and for the development of microangiopathy 55 patients with non-insulin-dependent diabetes mellitus (NIDDM) were studied. A 1 hr oral glucose tolerance test was performed at diagnosis and 5-10 yr later. At diagnosis all patients were free of microangiopathy, at reassessment 24 patients had evidence of microangiopathy, i.e. retinopathy, neuropathy or nephropathy, alone or in combination. The glucose induced increments of insulin levels (delta IRI) at reassessment correlated inversely with the degree of diabetic control, measured by Haemoglobin A1 (r = -0.466, p less than 0.01), and with the mean fasting blood glucose throughout the follow up period (r = -0.491, p less than 0.01). delta IRI at diagnosis was similar in patients with and without microangiopathy, and at reassessment, although lower in the microangiopathy group (11.2 +/- 2.1 vs. 16.4 +/- 2.1 microunits/ml, p less than 0.1). The difference between the 2 groups did not reach statistical significance. When patients were separated into those treated with diet alone and those treated with oral antidiabetic agents, delta IRI at reassessment was significantly lower in patients on oral agents (10.5 +/- 1.9 vs. 17.2 +/- 2.2 microunits ml, p less than 0.01), but the prevalence of microangiopathy was not different between 2 groups (37% and 52%, respectively). These findings show that in patients with NIDDM the residual beta cell function is important for the degree of diabetic control, but a direct relationship between the degree of insulin deficiency and the presence of diabetic microangiopathy is not established.
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PMID:Insulin secretory response to oral glucose load, diabetic microangiopathy and diabetic control: a study in non-insulin dependent diabetics. 675 36

Glucose tolerance tends to decrease in healthy aged subjects without family history of diabetes. Either reduced insulin secretion or insulin resistance may be responsible. Insulin secretion and insulin sensitivity were studied in 7 aged subjects (68-75 years) and 8 young controls (21-27 years). A 1-mg i.v. glucagon and a 5-U/m2 body area i.v. insulin test were run in each subject at 07(00) and at 19(00) on two different days to detect diurnal variations. An arginine test was also performed to evaluate pancreatic glucagon behavior. In the evening, young subjects presented a glucose tolerance impairment with significantly decreased plasma insulin levels, and a reduced hypoglycemic effect of exogenous insulin. Resistance to both endogenous and exogenous insulin in the aged was observed in the morning without significant morning/evening variations. Since the response to contra-insular hormones (GH in the insulin test, glucagon in the arginine test) was the same in both age groups, their role in the phenomenon could be ruled out. It is suggested that in the aged a stable reduction in number and/or a change in affinity of insulin receptors may occur. In addition, since aging is seen to be associated with the disappearance of diurnal variations in glucose tolerance and insulin secretion and sensitivity, and since a reduction in the receptor level of young healthy subjects in the evening has been reported by some authors, it is suggested that aged subjects may be less able to modulate the binding of insulin to its peripheral receptors in the course of the day.
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PMID:Diurnal variations in insulin secretion and insulin sensitivity in aged subjects. 700 42

In vitro, truncated glucagon-like peptides [GLP-1(7-36)-amide and GLP-1(7-37)] increase insulin secretion in a glucose-dependent manner, and desensitization to the action of GLP-1(7-37) has been demonstrated acutely with high concentrations. The purpose of these studies was to evaluate the glucose dependency and threshold of GLP-1(7-37) action in normal rats and in a rat model of type II diabetes and to assess the effects of long-term administration in vivo. All studies were conducted in conscious catheterized rats. An intravenous (IV) infusion of GLP-1(7-37) at 0.5, 5, or 50 pmol/min/kg during the second hour of a 2-hour 11-mmol/L hyperglycemic clamp in Sprague-Dawley rats produced a dose-related enhancement of the glucose-induced increase in plasma insulin concentration. A 1-hour infusion of a submaximal dose of GLP-1(7-37) (5 pmol/min/kg IV) in fasted and fed Sprague-Dawley rats produced small transient increases in plasma insulin (incremental increases above basal, 72 +/- 27 and 96 +/- 28 pmol/L, respectively) and decreases in plasma glucose (to levels > or = 5.2 mmol/L). Infusion of GLP-1(7-37) (5 pmol/min/kg IV) during a hyperglycemic clamp at two sequentially increasing concentrations of glucose, 11 and 17 mmol/L, produced incremental increases in insulin of 600 and 1,200 pmol/L, respectively, relative to levels in clamped control rats. Similarly, infusion of GLP-1(7-37) (5 pmol/min/kg IV) in hyperinsulinemic, hyperglycemic Zucker diabetic fatty (ZDF) rats produced a transitory increase in plasma insulin concentration and normalized the plasma glucose concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucose-dependent action of glucagon-like peptide-1 (7-37) in vivo during short- or long-term administration. 766


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