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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report on a 33-year-old patient from Sri Lanka who had been suffering from recurrent episodes of abdominal cramps since he was ten years old. He additionally suffered from postprandial flatulence and an increased frequency of bowel movements. By the age of 24, his condition had worsened with polyuria and polydipsia and he was diagnosed with type II diabetes mellitus. Recently, the patient's compliance deteriorated steadily and his diabetes mellitus was uncontrolled. His flatulence continued and he had six to seven bowel movements daily. He presented to us with renewed bouts of severe stomach cramps, similar to the painful episodes that the patient experienced in his youth. After exclusion of other etiologies and judging by the clinical picture, the patient's origin and the sonographically and radiologically verified pancreatic calcification, we rendered the diagnosis of a tropic calcifying pancreatitis with secondary diabetes mellitus. According to the literature, malignant neoplasia may develop on the basis of this disease. However, we were able to rule out a carcinoma as the cause of the current pain episodes in this patient based on clinical findings and course. We attributed the stomach cramps to compression of the common bile duct by the fibrotic head of pancreas. Pain and cholestasis regressed, thus obviating the need for surgical intervention (pancreaticojejunostomy). On therapy with enzyme substitution and insulin, the patient's exo- and endocrine pancreatic insufficiency was asymptomatic.
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PMID:[Chronic abdominal pain in a young diabetic patient]. 1111 10

Reduced exocrine pancreatic function has been observed in a high percentage of patients with type 1 diabetes in the past. There are only few data for type 2 diabetes available and they are contradictory. In this study we investigated exocrine pancreatic function in 105 controls and 114 patients with type 1 or type 2 diabetes mellitus by means of an indirect test (faecal elastase-1 concentration). This test has good sensitivity and specificity for moderate and severe pancreatic insufficiency as compared to the gold standard. Reduced faecal elastase-1 concentrations were found in 56.7% of type 1 patients, 35% of type 2 patients and 18.1% of the controls. Elastase-1 concentrations did not correlate with alcohol consumption, diabetes duration or diabetes therapy. The data found for type 1 patients correspond to those reported in earlier studies. The results for type 2 diabetics show that exocrine pancreatic function is also impaired in a high percentage in this group of patients. Pathogenetic concepts to explain these findings as consequences of diabetes complications or insulin deficiency are still under debate. Observations from autopsies and the data of the controls in this study suggest that chronic pancreatitis might be a common problem. In consequence, diabetes secondary to exocrine disease could be much more frequent than believed so far.
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PMID:Pancreatic exocrine function in patients with type 1 and type 2 diabetes mellitus. 1127 9

Despite the manageability of diabetes mellitus, complications associated with the disorder necessitate novel approaches to prevent immune-mediated impairment and destruction in type 1 diabetes, as well as the pancreatic insufficiency and peripheral resistance to insulin in type 2 diabetes. Islet transplantation is evolving into a clinical reality to treat type 1 diabetics and novel uses of gene engineering technology promise to result in tolerance to auto-, allo- and xenoantigens as well as microenvironment-specific immunosuppression. Through the use of a variety of gene delivery vehides, an increasing number of studies demonstrate the feasibility of shielding islet transplants and surrogate beta cells from immune rejection by the local secretion of immunosuppressive soluble molecules and anti-apoptotic factors. Although the achievements of gene and cell therapy in type 2 diabetes mellitus are less clear, seminal studies demonstrate the relevance of this approach to the treatment and perhaps prevention of the underlying causes of the disease, including obesity and insulin resistance. In this review, we attempt to illustrate pivotal studies demonstrating the suitability of genes and cells as drugs in type 1 and type 2 diabetes mellitus, and also provide some other targets that may be suitable for clinical utility.
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PMID:Genes and engineered cells as drugs for type I and type II diabetes mellitus therapy and prevention. 1209 May 47

Ultrastructural observations reveal a continuous interstitial matrix connection between the endocrine and exocrine pancreas, which is lost due to fibrosis in rodent models and humans with type 2 diabetes mellitus (T2DM). Widening of the islet-exocrine interface appears to result in loss of desmosomes and adherens junctions between islet and acinar cells and is associated with hypercellularity consisting of pericytes and inflammatory cells in T2DM pancreatic tissue. Organized fibrillar collagen was closely associated with pericytes, which are known to differentiate into myofibroblasts-pancreatic stellate cells. Of importance, some pericyte cellular processes traverse both the connecting islet-exocrine interface and the endoacinar interstitium of the exocrine pancreas. Loss of cellular paracrine communication and extracellular matrix remodeling fibrosis in young animal models and humans may result in a dysfunctional insulino-acinar-ductal-incretin gut hormone axis, resulting in pancreatic insufficiency and glucagon-like peptide deficiency, which are known to exist in prediabetes and overt T2DM in humans.
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PMID:Attenuation of endocrine-exocrine pancreatic communication in type 2 diabetes: pancreatic extracellular matrix ultrastructural abnormalities. 1904 May 93

Patients with cystic fibrosis are frequently affected with pancreatic insufficiency and are predisposed to the development of diabetes mellitus (DM) and bone demineralization. Cystic fibrosis-related diabetes mellitus is a clinical entity distinct from type 1 and type 2 diabetes, with important implications for the nutritional and pulmonary health of cystic fibrosis patients. This form of diabetes owes largely to insulin deficiency, but alterations in insulin sensitivity and hepatic glucose production have also been described. Therapy for cystic fibrosis-related diabetes differs substantially from type 2 DM, with careful attention to prandial glycemic excursions crucial to controlling its metabolic effects. Bone disease, including osteopenia and osteoporosis, also occurs with increased frequency in cystic fibrosis, owing to defects in intestinal absorption, chronic inflammation, lung disease, low body weight, and gonadal dysfunction. The pathogenesis, implications, diagnosis, and therapy of cystic fibrosis-related bone demineralization are discussed, with attention to recommended approaches to prevention of and treatment of established bone disease.
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PMID:Diabetes mellitus and bone disease in cystic fibrosis. 1976 May 39

Type 2 diabetes mellitus (T2DM) has been shown to be characterised by an almost abolished incretin effect. The incretin effect refers to the phenomenon of oral glucose eliciting a higher insulin response than intravenous glucose at identical plasma glucose profiles. It is conveyed by the two insulinotropic incretin hormones: glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). GLP-1 and GIP are secreted from the small intestines in response to ingestion of nutrients. The incretin defect of T2DM has been characterised by a virtually lost insulinotropic effect of GIP. It is unknown whether the incretin defect is a primary event leading to T2DM or arises as a consequence of the diabetic state. To investigate this we studied patients with chronic pancreatitis (CP). Over time, CP leads to secondary diabetes mellitus (DM). If patients with CP and secondary DM exhibit the characteristic type 2 diabetic incretin deficiencies and patients with CP and normal glucose tolerance are normal in that regard, it is more likely that these deficiencies are consequences of the diabetic state rather than primary events leading to T2DM. On the other hand, if incretin physiology is preserved independently of the endocrine status of patients with CP, the incretin defect could represent a primary pathogenetic defect. Three protocols have been employed to investigate this. In a study investigating postprandial incretin responses in 8 patients with CP and exocrine pancreatic insufficiency, with and without pancreatic enzyme supplementation (PES), we observed preserved incretin responses as compared to matched healthy subjects; and, further, that PES increased postprandial incretin responses in these patients. This suggests not only that the secretion of incretin hormones is regulated by the mere presence of nutrients in the small intestine, but also that the assimilation of such nutrients is involved, as well. Furthermore, we gauged the incretin effect in 8 patients with CP and normal glucose tolerance and in 8 patients with CP and secondary DM. Eight healthy subjects and 8 patients with T2DM were studied for comparison. The incretin effect was shown to be preserved in normal glucose tolerant patients with CP, whereas it was strongly reduced in patients with CP and secondary DM, suggesting the incretin defect to be a consequence of the diabetic state. Lastly, we investigated the insulinotropic effect of the incretin hormones in 8 patients with CP and normal glucose tolerance and in 8 patients with secondary DM, and observed that patients with CP and secondary DM exhibit an impaired insulinotropic effect of GIP, and that this most likely occurs as a consequence of the diabetic state. In conclusion, we suggest that: 1) the postprandial secretion of incretin hormones is preserved among patients with CP; 2) assimilation of nutrients stimulates secretion of GIP and GLP-1; and 3) the characteristic incretin deficiencies of T2DM most likely are consequences of a deteriorating glucose homeostasis, rather than primary events leading to T2DM.
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PMID:Incretin hormones and beta cell function in chronic pancreatitis. 2059 45

Pancreatic exocrine insufficiency is a frequently observed phenomenon in type 1 and type 2 diabetes mellitus. Alterations of exocrine pancreatic morphology can also be found frequently in diabetic patients. Several hypotheses try to explain these findings, including lack of insulin as a trophic factor for exocrine tissue, changes in secretion and/or action of other islet hormones, and autoimmunity against common endocrine and exocrine antigens. Another explanation might be that diabetes mellitus could also be a consequence of underlying pancreatic diseases (e.g., chronic pancreatitis). Another pathophysiological concept proposes the functional and morphological alterations as a consequence of diabetic neuropathy. This paper discusses the currently available studies on this subject and tries to provide an overview of the current concepts of exocrine pancreatic insufficiency in diabetes mellitus.
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PMID:Exocrine pancreatic insufficiency in diabetes mellitus: a complication of diabetic neuropathy or a different type of diabetes? 2182 21

Diabetes secondary to pancreatic diseases is commonly referred to as pancreatogenic diabetes or type 3c diabetes mellitus. It is a clinically relevant condition with a prevalence of 5%-10% among all diabetic subjects in Western populations. In nearly 80% of all type 3c diabetes mellitus cases, chronic pancreatitis seems to be the underlying disease. The prevalence and clinical importance of diabetes secondary to chronic pancreatitis has certainly been underestimated and underappreciated so far. In contrast to the management of type 1 or type 2 diabetes mellitus, the endocrinopathy in type 3c is very complex. The course of the disease is complicated by additional present comorbidities such as maldigestion and concomitant qualitative malnutrition. General awareness that patients with known and/or clinically overt chronic pancreatitis will develop type 3c diabetes mellitus (up to 90% of all cases) is rather good. However, in a patient first presenting with diabetes mellitus, chronic pancreatitis as a potential causative condition is seldom considered. Thus many patients are misdiagnosed. The failure to correctly diagnose type 3 diabetes mellitus leads to a failure to implement an appropriate medical therapy. In patients with type 3c diabetes mellitus treating exocrine pancreatic insufficiency, preventing or treating a lack of fat-soluble vitamins (especially vitamin D) and restoring impaired fat hydrolysis and incretin secretion are key-features of medical therapy.
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PMID:Diagnosis and treatment of diabetes mellitus in chronic pancreatitis. 2425 58

As the average life expectancy of patients with cystic fibrosis (CF) improves, the long term co-morbidities assume increasing importance. CF related diabetes (CFRD) has adverse effects on both nutrition and pulmonary function, and is associated with increased mortality. Abnormalities of glucose metabolism in CF represent a continuum; however the predominant abnormality is postprandial, not pre-prandial, glycemia. Insulin is currently recommended as the treatment of choice for CFRD, but its use is associated with a number of limitations, including hypoglycemia. Both the rate of gastric emptying and the consequent release of the 'incretin' hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like-peptide-1 (GLP-1), from the gut are important determinants of overall glycemic control, particularly postprandial glycemia. Both are abnormal in conditions associated with exocrine pancreatic insufficiency. Incretin based therapies that have the capacity to slow gastric emptying and/or modulate the release of 'incretin' hormones, are now used widely in type 2 diabetes (T2D). This paper explores the determinants of glycemic control in CF, with a particular focus on the roles of gastric emptying and 'incretin' hormones, providing a rationale for the use of therapies that delay gastric emptying, including incretin mimetics, to minimize postprandial glycemia and improve nutritional status.
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PMID:Cystic fibrosis related diabetes--a new perspective on the optimal management of postprandial glycemia. 2506 May 30

As care for the childhood cancer patient has improved significantly, there is an increasing incidence of treatment-related late effects. Obesity and type 2 diabetes mellitus are common and significant metabolic conditions in some populations of adult survivors of childhood cancer. Results from the Childhood Cancer Survivor Study and other large cohorts of childhood cancer survivors reveal that long-term survivors of acute lymphoblastic leukemia and those who received total body irradiation or abdominal radiotherapy are at highest risk. The potential mechanisms for the observed increase in risk, including alterations in leptin and adiponectin, pancreatic insufficiency, poor dietary habits, sedentary lifestyle, and perhaps changes in the composition of the gut microbiota, are reviewed. Discussion of exercise and diet intervention studies shows that further research about the barriers to a healthy lifestyle and other interventions in childhood cancer survivors is warranted.
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PMID:Obesity and Metabolic Disease After Childhood Cancer. 2656 32


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