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)

A 10-allele polymorphism was identified in rad (ras associated with diabetes), a gene that is overexpressed in non-insulin-dependent diabetes mellitus (NIDDM) muscle. The polymorphism, designated RAD1, consists of a variable number of trinucleotide repeats (GTT and ATT) located in the poly(A) region of an intronic Alu sequence. Based on the number of GTT and ATT repetitions, the alleles can be grouped into four classes (I-IV). RAD1 allele frequencies were determined in 210 NIDDM patients and 133 nondiabetic control subjects, all Caucasians. One allele (number 8, class III) accounted for > 80% of the chromosomes in both groups. However, an excess of minor alleles, all belonging to class I, II, or IV, was observed among NIDDM chromosomes (P < 0.025), suggesting a possible association between RAD1 and NIDDM predisposition. To promote further studies to test the hypothesis that genetic variability at the rad locus contributes to NIDDM, we mapped rad on the human genome. Using the fluorescence in situ chromosomal hybridization technique, rad was unequivocally assigned to chromosomal band 16q22. In families that were informative for RAD1, the rad locus was mapped within a 3-cM region defined by the markers D16S265, D16S186, and D16S397 (logarithm of odds scores = 10.08, 10.9, and 10.84 at recombination fractions of 0.024, 0.001, and 0.03, respectively). The high degree of heterozygosity of these markers will allow large-scale family studies to be performed to test the presence of linkage between rad and NIDDM.
Diabetes 1995 Feb
PMID:Trinucleotide repeats at the rad locus. Allele distributions in NIDDM and mapping to a 3-cM region on chromosome 16q. 785 47

The usefulness of fasting plasma glucose (FPG) in the diagnosis of diabetes mellitus was assessed in Asian Indians in South India. Oral GTT values in 570 newly screened adults were studied. Taking the WHO criteria of 2 h plasma glucose (PG) of > or = 11.1 mmol l-1 for diagnosis of diabetes, the validity of a FPG of > or = 7.8 mmol l-1 cut off value for diabetes was assessed. Using the regression analysis, the correlations of the FPG to 2 h PG were examined. Among the 268 with 2h PG value of > or = 11.1 mmol l-1, 205 (76.5%) had FPG > or = 7.8 mmol l-1. Sensitivity of FPG was 76.5% for diagnosis of diabetes and its specificity was 99%. An exponential regression model gave the best fit for FPG vs 2 h PG and using the regression equation, the predicted FPG for a 2 h PG of 11.1 mmol l-1 was 7.05 mmol l-1. Sensitivity increased to 90.3% with FPG of 7.05 mmol l-1 while the specificity remained at 92%. It is concluded that in the south Indian subjects, the sensitivity for diagnosis of diabetes with FPG of > or = 7.8 mmol l-1 was 76.5%; and it increased to 90.3% with FPG of > or = 7.05 mmol l-1.
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PMID:Fasting plasma glucose in the diagnosis of diabetes mellitus: a study from southern India. 828 24

Vitamin D is essential for normal insulin secretion in vivo and in vitro. The differential effect of calcium and of the vitamin D endocrine system in the insulin response to secretagogues is still a subject of debate. To study the roles of calcium and the vitamin D system in the in vivo insulin response, GTT and insulin sensitivity tests were conducted in rats presenting vitamin D depletion and hypocalcemia or vitamin D depletion supplemented with calcium alone for 3, 7, or 14 days, vitamin D3 (6.5 nmol/day x 7 days), or 1,25(OH)2D3 (28 pmol/day x 7 days). Serum calcium was 1.28 +/- 0.04 mM in hypocalcemic vitamin D-depleted rats, 1.47 +/- 0.06 (NS), 1.8 +/- 0.2 (P < 0.0002), and 2.04 +/- 0.07 (P < 0.0001) mM after 3, 7, or 14 days, respectively, of calcium supplementation; vitamin D3- or 1,25(OH)2D3-supplemented animals had serum calcium of 2.61 +/- 0.04 or 2.48 +/- 0.05 mM (P < 0.0001 vs. hypocalcemic vitamin D-depleted rats). Rats with hypocalcemia and vitamin D depletion had significantly higher glucose concentrations (P < 0.0005) and lower insulin response during GTT than all other groups (P < 0.001). Differences in insulin sensitivity could not account for differences in response because exogenous insulin administration led to a similar drop in glucose concentrations in all groups, with the nadir averaging 51.7 +/- 2.6% of initial values. To distinguish between calcium and the vitamin D system in the GTT response, rats were treated with a nonhypercalcemic analogue of 1,25(OH)2D3, OCT (28 pmol/day x 4-7 days) with or without dietary calcium.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1993 Jan
PMID:Calcium is essential in normalizing intolerance to glucose that accompanies vitamin D depletion in vivo. 838 May 63

The major cause of primary nonfunction of transplanted islets is nonspecific inflammation associated with the transplantation procedures. Using mouse islet isografts, we attempted to prevent graft loss mediated by nonspecific inflammation using recipient treatment with nicotinamide (NA) and 15-deoxyspergualin (DSG). Newborn BALB/c islets, ranging in numbers between 1200 and 1500, were transplanted into syngeneic adult mice made diabetic by intravenous injection of 200 mg/kg streptozotocin. Recipient mice were divided into the following four groups, based on the treatment protocol of NA and DSG: intraperitoneal injection (IP) of normal saline (Group 1), IP injection of 2500 mg/kg NA (Group 2), IP injection of 5 mg/kg DSG (Group 3), and IP injection of NA + DSG (Group 4). Treatment started Day -1 and continued until Day 9 (Day 0 is day of transplantation). Blood and urine glucose, body weight, and intravenous glucose tolerance tests (IV-GTT) were examined after transplantation. Reversal of diabetes, as indicated by normoglycemia and negative urine glucose, was higher in Groups 2 (75%), 3 (50%), and 4 (85.7%), compared to Group 1 (11.1%). Especially in Group 4, the endocrine function and morphology of grafted islets were well preserved as shown by K values of IV-GTT and histological studies. These results suggest the importance of islet protection from irreversible damage by nonspecific inflammation at earlier stages of implantation, and the effectiveness of a short course of treatment with NA and DSG.
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PMID:Protection of mouse islet isografts from nonspecific inflammatory damage by recipient treatment with nicotinamide and 15-deoxyspergualin. 866 75

If the patient showed borderline glucose intolerance (BGI), they used to be treated as a diabetic. However, as the uterus expands during pregnancy, excretion from the stomach is disturbed and the frequency of BGI increases. If GTT is performed for pregnant women, frequency of BGI increase up to 50% and BGI does not mean glucose intolerance during pregnancy. Instead of BGI, gestational diabetes mellitus demonstrates glucose intolerance during pregnancy. Gestational diabetes develops diabetes frequently after delivery and requires strict Follow-up.
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PMID:[Abnormal carbohydrate metabolism during pregnancy]. 891 44

This study was made to analyze predictive NIDDM markers using a long-term GTT follow-up observation period of 1-30 years. Subjects of this study were 5446 cases (3994 males, 1452 females). Results are as follows: (1) NIDDM development rate increased gradually with increasing 2 h-PG levels at GTT, but for groups with 2 h-PG > or = 170 mg/dl, the rate rose rapidly. (2) PG at GTT was higher in the NIDDM development group than in the control group. Mean 1 h-PG reached > or = 200 mg/dl for 4 years before onset in the NIDDM group. Frequency of 1 h-PG > or = 200 mg/dl was 54% 4 years before and 67% 1 year before onset. (3) The highest NIDDM prediction accuracy was in 1 h-PG levels of 200 mg/dl or more and/or 2 h-PG levels of 170 mg/dl or more. Sensitivity was 75.2%, and specificity, 63.4% within 3 years before onset. (4) With addition of delta IRI/delta PG, sensitivity increased, but specificity decreased. (5) The highest relationship with NIDDM development was for high PG levels (1 h-PG > or = 200 mg/dl and/or 2 h-PG > or = 170 mg/dl), the odds ratio being 5.65. The odds ratio of delta IRI/delta PG was lower than ratio of high PG levels. (6) NIDDM development rate increased about 50% in the under-60-years age group and in the group of BMI > or = 25.
Diabetes Res Clin Pract 1996 Oct
PMID:Prediction of diabetes mellitus (NIDDM). 901 64

Hypoglycaemic effect of a Neapalese plant Biophytum sensitivum was investigated in the alloxan diabetic male rabbits of different severities: subdiabetic (Alloxan recovered; AR), mild diabetic (MD) and severely diabetic (SD). Assessment of activity of the extract, prepared from the plant leaves, was done by fall in fasting plasma glucose (FPG) and improvement in the oral glucose tolerance test (OGTT), following single dose and prolonged administrations. Following single dose administration there was fall in 1 hour and 2.5 hour glucose values by 25.9% and 27.4% respectively in the subdiabetic rabbits, and by 36.9% and 37.7% in the mild diabetic rabbits. Improved GTT response is shown by fall in area under curve (AUC) from 16138 mg/dl to 12355 mg/dl (23.4%) in the subdiabetic rabbits, and from 19258 to 12238 mg/dl in the MD rabbits. More significant improvements occurred following one week of above treatment. The results prove that the plant material has significant hypoglycaemic effect, which is possibly due to pancreatic beta-cell stimulating action. To investigate its possible role in correction of other metabolic abnormalities of diabetes further long term studies are required.
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PMID:Hypoglycemic effect of Biophytum sensitivum in the alloxan diabetic rabbits. 974 56

This study was done in adult offspring of two diabetic (NIDDM) parents (ODP) to look for changes in specific insulin (insulin) and proinsulin responses due to strong familial background and also in different states of glucose intolerance. Equal numbers (20 in each group) of ODP with normal glucose tolerance (NGT), impaired glucose tolerance (IGT) and diabetes (DM) were chosen. Twenty, age and BMI matched healthy controls, without family history of diabetes, were also studied for comparison. Plasma specific insulin and proinsulin were measured by radioimmunoassays in fasting and 120' plasma samples collected during the GTT. Proinsulin to insulin ratio were calculated. Insulin resistance (IR-HOMA) was calculated. In NGT, fasting proinsulin-insulin ratio was significantly higher than the control value (P = 0.023). Insulin values at 120' was higher than control values, though it did not reach statistical significance. Proinsulin at 120' was higher than controls (P = 0.016). In IGT, the fasting proinsulin to insulin ratio, the 120' proinsulin and insulin values were higher than controls (P = 0.048, 0.0013 and 0.0001, respectively). Fasting proinsulin-insulin ratio in IGT was similar to the value in NGT. In diabetic subjects proinsulin concentrations were significantly higher than controls at fasting (P = 0.0004), and 120' (P = 0.0007). The fasting values were higher compared to NGT also (P = 0.037). Proinsulin-insulin ratios were higher than the values in controls (P = 0.0008), IGT (P = 0.047) and NGT (P = 0.05). Diabetic subjects had higher fasting insulin values compared to the control values although between the groups no statistical significance was found (P = 0.22 by Kruscall Wallis test). At 120' both insulin and proinsulin values increased from NGT to IGT, but with development of diabetes a reduction was seen in the responses. Insulin resistance (IR-HOMA) increased steadily from NGT to diabetes. The difference between NGT and controls in IR was not statistically significant. This study of Asian Indian offspring of diabetic parents has shown that genetic predisposition to diabetes resulted in increased proinsulin to insulin ratio at the fasting state. Absolute hyperproinsulinaemia occurred only with development of diabetes.
Diabetes Res Clin Pract 1998 Jul
PMID:Effects of genetic predisposition on proinsulin responses in Asian Indians. 976 75

Islets isolated from rats fed a lipid-enriched diet have shown an impairment of insulin secretion, but there is no available data comparing the effect of diet containing different dietary fat. This may be important in preventing or facilitating the establishment of diabetes. In this study, the effect of diets enriched (10%) with different fatty acids on insulin secretion by isolated pancreatic islets was investigated. The sources of the fatty acids tested were: saturated long chain from animal fat (AF), polyunsaturated from soybean oil (SO), and monounsaturated from olive oil (OL). The results were compared with those from rats receiving a diet enriched (10%) with a balanced mixture of fatty acids (the same proportion of AF, SO, and OL). The effect of fat-rich diets on insulin release was tested in vivo by giving a glucose load (glucose tolerance test-GTT) and in vitro in perfused islets. The mechanism involved was also examined by measuring 45Ca2+ and 86Rb+ fluxes, GLUT-2 content, and glucose oxidation in isolated islets. A significant increase of insulin secretion and glucose oxidation without any alteration of the ionic movements were detected in islets from SO and OL rats. GLUT-2 content was increased in islets of the OL group but diminished in AF rats. The results led us to postulate that soybean and olive oils may increase the response of insulin secretion to glucose stimulus in pancreatic islets.
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PMID:Soybean- and olive-oils-enriched diets increase insulin secretion to glucose stimulus in isolated pancreatic rat islets. 985 78

A combined (GTT)n (ATT)n trinucleotide-repeat polymorphism designated as RAD1 has been identified at intron 2 of the rad gene on chromosome 16q. An association between the total length of the RAD1 locus and type 2 diabetes has been shown in white American subjects, but not in Finns. We genotyped 115 Japanese patients with type 2 diabetes and 114 nondiabetic control subjects at the RAD1 locus by the direct sequencing method, and found 16 RAD1 alleles composed of various combinations of GTTs and ATTs. Allele 14 consisting of four GTTs and seven ATTs accounted for the majority in both control subjects and diabetic patients, suggesting that RAD1 polymorphism is not a major genetic component for susceptibility to common forms of diabetes in the Japanese. There was no significant association between total repeat length and diabetes. However, the frequency of minor alleles containing five GTTs or three GTTs was significantly higher in diabetic patients versus nondiabetic subjects (4.8% v 0.9%, P = .012). Thus, genetic variability at the rad gene in linkage disequilibrium with RAD1 could be associated with a predisposition to type 2 diabetes in the Japanese population.
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PMID:Analysis of trinucleotide-repeat combination polymorphism at the rad gene in patients with type 2 diabetes mellitus. 1002 77


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