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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cats are one of the few species that develop a form of diabetes mellitus that is clinically and histologically analogous to human type 2 diabetes mellitus. Figure 9 summarizes the etiologic factors thought to be involved in the development of feline and human type 2 diabetes. The main metabolic characteristics of type 2 diabetes mellitus are impaired insulin secretion and resistance to the action of insulin in its target tissues. Impaired beta cell function occurs before histologic changes become evident. The characteristic histologic finding in cats with type 2 diabetes is deposition of amyloid in pancreatic islets. Amyloid deposition occurs before the onset of clinical signs, but does not seem to be the primary defect. Pancreatic amyloid is derived form the recently discovered pancreatic hormone amylin. Amylin is synthesized in pancreatic beta cells, and is co-stored and co-secreted with insulin. Amylin has been postulated to be involved in the pathogenesis of feline diabetes mellitus both through its metabolic effects, which include inhibition of insulin secretion and induction of insulin resistance, and via progressive amyloid deposition and beta cell degeneration. Increased amylin concentration has been documented intracellularly in cats with impaired glucose tolerance and in the plasma of diabetic cats, and supports the hypothesis that amylin is involved in the pathogenesis of type 2 diabetes. Obesity is a common finding in diabetic felines and is a contributing factor to the insulin resistance present in type 2 diabetes. Clinical signs of diabetes develop once total insulin secretion decreases to 20% to 25% of normal levels. Many diabetic cats have been treated successfully with oral hypoglycemics, but 50% to 70% of diabetic cats are insulin dependent. Based on histologic evidence, this is the result of extensive amyloid deposition and subsequent beta cell degeneration, rather than autoimmune destruction of pancreatic beta cells associated with type 1 diabetes. Alternative ways of treating type 2 diabetes currently are being investigated. Amylin antagonists recently have been proposed as a novel treatment to reverse the deleterious effects of excessive amylin concentrations. The gastrointestinal hormone glucagon-like peptide-1 may also prove useful in treating diabetic cats, because of its stimulatory effect on insulin secretion and synthesis, and the absence of significant hypoglycemic effect.
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PMID:Pathogenesis of feline diabetes mellitus. 766 May 30

Quite different nutrition-related environmental factors influence the development of type 1 insulin-dependent diabetes (IDDM) and type 2 non-insulin-dependent diabetes (NIDDM). IDDM is characterized by progressive beta-cell destruction which leads to complete insulin deficiency; at the time of diagnosis 80-90% of beta cells have been destroyed. In children there is epidemiological evidence that high intake of nitrites and N-nitroso compounds, early introduction of cow's milk to the diet and short duration or absence of breastfeeding increase the risk of IDDM. Studies in experimental animals suggest that cow's milk and soy proteins may be diabetogenic. There is current interest in the effects of free radical scavengers, particularly niacin and natural and synthetic antioxidants on the incidence of IDDM. These findings from ecological, animal, and human case-control studies remain to be evaluated in prospective cohort studies covering infancy and childhood and finally in human intervention trials. NIDDM is characterized by insulin resistance which is complicated by impaired insulin secretion at the time of appearance of hyperglycaemia and clinical diabetes. Its preclinical development is insidious and poorly defined, and there is little direct evidence that the same factors which influence metabolic control in clinical diabetes also affect the preclinical development of the disorder. Obesity, particularly of the abdominal type, is common in people who develop NIDDM, and weight control by appropriate diet and physical activity is probably the most important measure for preventing NIDDM. High (saturated) fat intake seems to be associated with insulin resistance, obesity and increased risk of NIDDM, and diets high in carbohydrate seem to protect from glucose intolerance and diabetes, mainly owing to their high fibre content.
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PMID:Dietary factors in the aetiology of diabetes. 769 75

The levels of glucose, insulin, and C-peptide in the blood serum were measured in 38 subjects with normal and impaired glucose tolerance whose parents suffered from insulin-dependent and noninsulin-dependent diabetes mellitus (IDDM and NIDDM, respectively) and in 12 normal subjects without hereditary aggravation for diabetes mellitus in order to specify the peculiarities of development of diabetes mellitus of various types. Reliably increased levels of glucose, insulin, and C-peptide on an empty stomach and absence of adequate secretion of insulin and C-peptide in response to stimulation with 5 mg of minidiab, expressed by a later and less manifest release of insulin and C-peptide, were observed in the test group, in contrast to healthy controls. The detected changes augment with the progress of carbohydrate metabolism disorders, being more marked in the subjects whose parents suffered from IDDM. The findings permit a conclusion that function of the insular system is changed during early disorders of carbohydrate metabolism in subjects whose parents suffered from both forms of diabetes mellitus. Minidiab test is recommended to specify the function of the pancreatic insular system.
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PMID:[Minidiab test to assess the functional state of pancreatic beta-cells in the children of diabetics]. 774 43

Insulin-dependent diabetes mellitus (IDDM) is a frequent complication in patients with beta-thalassaemia major. It is believed to be a consequence of the damage inflicted by iron overload to the pancreatic beta-cell. Liver disorders and genetic influences seem to be additional predisposing factors to diabetes mellitus in patients with beta-thalassaemia. Ethnic variations are frequently reported on prevalence and complications of diabetes mellitus in the beta-thalassaemia patients. We investigated 50 Saudi children (< 15 years) with beta-thalassaemia major and 50 beta-thalassaemia minor, and age- and sex-matched controls for the prevalence of diabetes mellitus, and its relation to hitherto claimed predisposing factors. Fasting blood glucose, plasma insulin level, liver function tests, plasma ferritin, iron, and transferrin were assessed in each patient and glucose tolerance was evaluated. Results in patients with beta-thalassaemia major were compared with those obtained for beta-thalassaemia minor and the controls. The results showed moderate elevation of ferritin level in the majority of the beta-thalassaemia major despite desferroxamine therapy. Either hyperinsulinaemia or hypoinsulinaemia was encountered in the majority of these patients. The prevalence of diabetes mellitus was 6 per cent compared to 2 per cent in the beta-thalassaemia minor and normal children. Impaired glucose tolerance (IGT) occurred at a significantly higher (24 per cent) frequency in the beta-thalassaemia major compared to 2 and 0 per cent in the beta-thalassaemia minor patients and normal controls, respectively. The prevalence of diabetes mellitus was significantly lower in the Saudi thalassaemic patients compared to the results obtained from patients of other ethnic groups reported in literature.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diabetes mellitus in children suffering from beta-thalassaemia. 780 19

Candidate genes for NIDDM have been screened in Japanese. Mutations in the glucokinase gene were found in apparent late-onset NIDDM patients as well as in MODY patients. Clinical characteristics in the subjects with glucokinase gene mutations are similar to those in Caucasian subjects; diabetes mellitus is generally mild and some patients actually remain as having impaired glucose tolerance. Of great interest is that all affected subjects show blunted insulin secretion response to the glucose challenge, which is most commonly observed in Japanese NIDDM patients. Thus, it is possible that impairment in the regulation of glucokinase gene expression or its enzyme activity is associated with at least some Japanese NIDDM patients, though the prevalence of the mutations in the coding region is relatively low. In contrast, a mitochondrial tRNA(Leu(UUR)) gene mutation at np 3243 appears to be much more common, and diabetes due to this mutation has a progressive nature. Insulin secretory capacity progressively decreases, eventually reaching an insulin-dependent state in most patients. A surprising result is that this gene mutation is often observed in ICA-positive IDDM patients who were initially non-insulin-dependent, so called slowly progressive IDDM patients. These results suggest that the mitochondrial gene mutation may cause beta cell loss in addition to defects in glucose-induced signaling in pancreatic beta cells, which explains that the mitochondrial gene mutation manifests a wide range of diabetic phenotypes, from NIDDM to IDDM.
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PMID:NIDDM--genetic marker; glucose transporter, glucokinase, and mitochondria gene. 785 92

By the cooperation of members of the Japan Diabetes Society, we collected data on 144 twin pairs with diabetes or glucose intolerance. By the diagnosis of reporting physicians, the concordance rate of diabetes in monozygotic twins (MZ) was 47% (9/10) for IDDM and 87% (68/78) for NIDDM. The concordance rate in dizygotic twins (DZ) was 8% (1/13) and 43% (9/21) for IDDM and NIDDM, respectively. The concordance rate was higher in MZ than in DZ and in IDDM than in NIDDM. In MZ, the concordance rate was higher in twin pairs in which probands developed diabetes at an older age. The discordant period for diabetes was not shorter in discordant pairs than in concordant pairs. The period of living together was irrelevant to concordance for diabetes. When co-twins of NIDDM twins were examined by oral glucose tolerance test, 98% of co-twins of MZ and 92% of co-twins of DZ had diabetes or a milder degree of glucose intolerance, while in IDDM pairs 45% of MZ and 50% of DZ co-twins had normal glucose tolerance. The insulinogenic index (the ratio of the increment of insulin to that of blood glucose 30 min after a glucose load) in discordant NIDDM co-twins was similar to subjects with the same degree of glucose intolerance.
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PMID:Diabetic twins in Japan. 785 35

The frequency of a positive family history of diabetes in diabetic patients has increased in recent studies. In this study, it was 16-33% for type 1 diabetes and 43-49% for type 2 diabetes. It was significantly higher than in non-diabetic subjects, and in type 2 than in type 1 diabetic patients. The prevalence of diabetes in parents and siblings of type 2 diabetic patients was higher than in those of type 1 patients, and it was particularly high in parents of young onset type 2 patients. Among type 2 diabetic patients, positive family history was somewhat lower in those with marked obesity in the past. Comparison of groups with varying degrees of glucose intolerance revealed that a family history of diabetes increased in parallel with the impairment of glucose tolerance. The results suggest that genetic factors in the pathogenesis of diabetes are more important in type 2 than in type 1 diabetes, and in the younger onset and less obese subjects than in older onset and more obese patients for type 2 diabetes.
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PMID:Family history of diabetic patients in Japan. 785 36

Although NIDDM is by far the most frequent form of diabetes, the pathogenesis is less clear and even more controversial than in IDDM. There is a heterogeneity of IDDM and NIDDM and there are reasons why the two types should be considered different diseases although we do not know exactly why. NIDDM is the result of a disbalance between insulin sensitivity and insulin secretion. Fully developed NIDDM syndrome calls for the concurrent existence of both main defects, i.e. insulin resistance and deteriorated B-cell function. It is important that the two defects must occur simultaneously, only then marked glucose intolerance develops. Concurrent hyperglycaemia and hyperinsulinaemia on fasting suggest severe insulin resistance. Investigations provide evidence that hyperinsulinaemia is a predictor of the final development of IGT and IDDM and it was demonstrated that hyperglycaemia is a predictor of development of NIDDM in Caucasians.
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PMID:[Recent findings on type II non-insulin-dependent diabetes (epidemiologic data, etiopathogenesis)]. 802 76

To learn more about the preclinical phase of IDDM we observed for a median period of 46.5 months (range 0.5-69 months) a group of 57 siblings positive for ICA and/or IAA when first screened within 6 months of the diagnosis of the proband. Sequential blood samples and IVGTTs were obtained at intervals of 6-12 months. Seventeen siblings (29.8%) presented with IDDM during the observation period. The duration of the known preclinical period ranged from 0.5 to 51 months (median 29 months). The converters were younger than the other siblings (P < 0.05) and had higher initial ICA levels (P < 0.01). In addition they had a lower FPIR in the first IVGTT (P < 0.001). On all subsequent tests the converters had higher ICA levels and a lower FPIR (P < 0.05 or less), a lower glucose elimination rate from the third test onwards (P < 0.01 or less) and higher IAA levels at 3 years (P < 0.05). Some variation could be observed in the FPIR in the converters with an initial increase and subsequent decrease (P < 0.05 for both). Their levels of complement-fixing ICA increased up to 18 months (P < 0.05) and IAA levels up to 3 years (P < 0.01). Those high risk siblings who progress to clinical IDDM are characterized by young age, strong and increasing signs of islet-cell specific autoimmunity, reduced insulin secreting capacity and emerging glucose intolerance. The present observations seem to be incompatible with the hypothesis of beta-cell destruction occurring at a constant, predictable rate.
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PMID:Natural history of preclinical IDDM in high risk siblings. Childhood Diabetes in Finland Study Group. 806 40

The pathogenetic mechanism underlying glucose intolerance in pancreatic cancer is still unclear. We studied the pattern of three glucose regulating hormones (C-peptide, glucagon and GH) in pancreatic cancer patients with (N = 34) and without (N = 8) hyperglycemia, and compared the findings made with those from subjects with other hyperglycemic conditions of well-known origin [type I diabetes mellitus (8 cases) and diabetes mellitus secondary to chronic pancreatitis (13 cases) or liver cirrhosis (4 cases)]. In hyperglycemic pancreatic cancer patients, C-peptide was absent in 26% of the cases, reduced in 24%, elevated in 29% and within the normal range in the remaining 21%. In normoglycemic pancreatic cancer this hormone was reduced in two cases (25%) and within the normal range in all the others. GH was within the normal range in all cases: glucagon was below the normal range in some hyperglycemic pancreatic cancer patients (41%) or within the normal range in all the remaining patients. No correlations were found between the three hormones when findings from subjects were considered all together. However, in pancreatic cancer C-peptide and glucagon presented consensual variations. C-peptide, glucagon and GH levels were not related to tumor volume; glucagon was found to be associated with liver metastases. C-peptide was correlated with serum ALT and ALP. We may conclude that hyperglycemia associated with pancreatic cancer may be caused by different mechanisms. In some cases a reduced secretion of both insulin and glucagon was observed, as occurs in chronic pancreatitis. In the majority of patients, beta cell function appears normal, and the hyperglycemic state may depend on an altered peripheral sensitivity to insulin due to the pancreatic pathology itself or to consensual liver involvement.
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PMID:C-peptide pattern in patients with pancreatic cancer. 813 97


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