Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate beta-cell function in patients with pancreatic cancer, the glucagon stimulation test was performed in seven patients with pancreatic adenocarcinoma, seven patients with type I diabetes mellitus, seven patients with type II diabetes mellitus, and in seven healthy controls. C-peptide serum levels were determined before and after a 1-mg i.v. glucagon injection. Basal C-peptide values were normal or slightly increased in pancreatic cancer and type II diabetic patients and low in type I diabetic patients. Following glucagon stimulation, no significant increase was observed in C-peptide values of type I diabetics and pancreatic cancer patients, whereas significant increases occurred in controls and type II diabetics. It is concluded that the altered beta-cell function found in pancreatic cancer patients may lead to hyperglycemia, which is frequently associated with this tumor type.
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PMID:Beta-cell function in pancreatic adenocarcinoma. 802 55

Although an association between diabetes and cancer was found over 100 years ago, the issue underwent different interpretations over the subsequent decades, and only modern, prospective, epidemiological cohort and case-control studies conducted in several countries have provided reliable evidence of an increased cancer risk in diabetic patients, mainly in those with type 2 diabetes. This risk varies according to the tumor site: it is the greatest for primary liver cancer, moderately elevated for pancreatic cancer, and relatively low for colorectal, endometrial, breast, and renal cancers. The cause of the association is not clear and remains the subject of different hypotheses. The most frequently cited reason is the potential effect of insulin. Found in high concentrations, due to insulin resistance in most patients with type 2 diabetes, this hormone is believed to express a mitogenic effect. This hypothesis needs to be confirmed in appropriately programmed prospective studies, but it may already be helpful in choosing an adequate treatment for type 2 diabetes to achieve optimal metabolic control with a simultaneous reduction in hyperinsulinemia, such as diet, physical exercise, metformin, and acarbose.
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PMID:Diabetes mellitus and cancer. 1102 48

The incidence of diabetes is increased in patients with pancreatic cancer, but the mechanisms underlying this association are not clear. Alterations in beta-cell function, such as formation of amyloid from excessive production of amylin and reduced expression of GLUT2, have been suggested to be possible mechanisms. We compared in vivo secretory responses of amylin and insulin (n = 37) and expression of GLUT2 in pancreata (n = 10) obtained at surgery between diabetic and nondiabetic patients with and without pancreatic tumors. Fourteen had pancreatic adenocarcinoma, 7 had diabetes (duration 6 +/- 3 years) and a pancreatic tumor, 8 had type 2 diabetes (duration 6 +/- 2 years), and 8 were normal subjects. First (0 to 10 minutes) and second (10 to 120 minutes) phase insulin and amylin secretion were characterized using the hyperglycemic clamp technique. Both amylin and insulin concentrations followed a biphasic pattern in nondiabetic subjects. In nondiabetic patients with pancreatic cancer, total, as well as nonglycosylated amylin concentrations, were increased compared with nondiabetic subjects without pancreatic cancer. Both first- and second-phase plasma amylin and serum immunoreactive insulin concentrations were low in all patients with diabetes, ie, both in type 2 diabetes and in those patients with diabetes and pancreatic tumors. At surgery, specimens were obtained for characterization of GLUT2 expression in beta cells, which was unaltered in nondiabetic (n = 7) and diabetic (n = 3) patients. Amyloid staining was similarly negative in diabetic and nondiabetic pancreata independent of pancreatic carcinoma. In conclusion, plasma amylin, but not insulin concentrations, are increased in nondiabetic patients with pancreatic cancer, but low in all patients with diabetes. These data support the potential of using an increase in the ratio of circulating amylin to insulin as a marker for pancreatic cancer in nondiabetic patients.
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PMID:In vivo glucose-stimulated amylin secretion is increased in nondiabetic patients with pancreatic cancer. 1155 35

Tropical chronic pancreatitis (TCP) is a juvenile form of chronic calcific non-alcoholic pancreatitis, seen almost exclusively in the developing countries of the tropical world. The classical triad of TCP consists of abdominal pain, steatorrhoea, and diabetes. When diabetes is present, the condition is called fibrocalculous pancreatic diabetes (FCPD) which is thus a later stage of TCP. Some of the distinctive features of TCP are younger age at onset, presence of large intraductal calculi, more aggressive course of the disease, and a high susceptibility to pancreatic cancer. Pancreatic calculi are the hallmark for the diagnosis of TCP and in non-calcific cases ductal dilation on endoscopic retrograde cholangiopancreatography, computed tomography, or ultrasound helps to identify the disease. Diabetes is usually quite severe and of the insulin requiring type, but ketosis is rare. Microvascular complications of diabetes occur as frequently as in type 2 diabetes but macrovascular complications are uncommon. Pancreatic enzyme supplements are used for relief of abdominal pain and reducing the symptoms related to steatorrhoea. Early diagnosis and better control of the endocrine and exocrine dysfunction could help to ensure better survival and improve the prognosis and quality of life of TCP patients.
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PMID:Tropical chronic pancreatitis. 1465 69

Risk of development of some gastrointestinal tract cancers (colorectal cancer, pancreas cancer and liver cancer) is higher in type II diabetics. Another important risk factor is obesity (for gall bladder cancer in women and in men also for stomach and esophageal cancer). Pathogenetic factors have been explored especially in colorectal cancer (diet, hyperinsulinaemia, metabolic receptors activation, absence of physical activity). Our Czech study also proved up to 4 times increased risk of colorectal cancer in diabetics and, in accordance with literature, probable influence of persistent diabetes on tumour development. Type II diabetes mellitus should be considered as a risk factor especially for colorectal cancer, liver cancer, and pancreas cancer. In type I diabetics no risk of gastrointestinal tract cancers was proved.
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PMID:[Gastrointestinal tract cancer and diabetes mellitus]. 1530 38

Findings obtained from numerous prospective cohort and case-control studies on alcohol consumption and pancreatic cancer risk have been inconsistent, with many confounding variables present in various investigations. However, heavy alcohol consumption has been known to be a major cause of chronic pancreatitis and a risk factor for type 2 diabetes mellitus, both of which are linked to pancreatic cancer. It has been established that an extensive normal interaction exists between the exocrine and endocrine pancreas, as well as in inflammatory processes and carcinogenesis. Alcohol and its metabolites (acetaldehyde and fatty acid ethyl esters) can alter metabolic pathways involved in the inflammatory response and carcinogenesis, and they are mediated by one or more of the following mechanisms: (1) premature activation of zymogens; (2) induction of the inflammatory response through activation of nuclear transcription factors, including nuclear factor-kappa and activation protein 1; (3) increased production of reactive oxygen species, resulting in oxidative DNA damage and altered effect of dietary antioxidants; (4) activation of pancreatic stellate cells, which leads to fibrosis; (5) gene mutation in enzymes related to cytochrome P450, glutathione S-transferase, aldehyde dehydrogenase, cationic trypsinogen, and pancreatic secretory trypsin inhibitor; (6) synergistic effects of ethanol and tobacco carcinogen on NNK [nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone] metabolism; and (7) dysregulation of proliferation and apoptosis. These various metabolic effects of alcohol can lead to or interact with other risk factors (genetic, dietary, environmental, and lifestyle factors) that result in acute and chronic pancreatitis and diabetes mellitus and, ultimately, affect the multistep process of carcinogenesis toward the development of pancreatic cancer.
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PMID:Alcohol and pancreatic cancer. 1605 82

The principal method of measuring total body water (TBW) is by isotope dilution. Also, the doubly labelled water method, which is the method of choice for measuring total energy expenditure (TEE) in free-living individuals, includes calculation of TBW as the dilution space of the tracer. TBW was measured in 261 subjects (135 males and 126 females), aged 3-87, including healthy children, children with HIV and adults with non-insulin dependent diabetes mellitus (type 2 diabetes), mild hypertension, pancreatic cancer and lung cancer, either in studies of body composition or TEE. A linear relationship was found between TBW and height in all subjects. When TBW is plotted against height cubed (Ht3, m3) the regression line can be forced through the origin. Considering only adults with 18.5>body mass index <29.9 and all children (n=220), this yielded TBW (l)=7.40 x Ht3, R2=0.95. This simple linear relationship between measured TBW and Ht3 compared favourably with other prediction methods, assuming TBW is a constant proportion (55%) of body weight and TBW predicted from height and weight (mean difference between measured and predicted TBW 0.55 l compared with -1.95 and -1.20 l, respectively). Absolute errors were greater at higher TBW, but use of a log10 transformation reduced this effect. This simple relationship of TBW with Ht3 is too crude to be used as a body composition predictor in individual subjects as it ignores, for instance, body shape. However, it can be used as a quality control tool. Here, use of a log10 transformation and residual plot can serve to identify outliers, which can be checked for gross errors in data input and if necessary samples are re-analysed.
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PMID:A simple prediction of total body water to aid quality control in isotope dilution studies in subjects 3-87 years of age. 1619 62

The incidence of hepatocellular carcinoma is increasing, but the temporal changes of risk factors remain unclear. A significant proportion of hepatocellular carcinoma (7-30%) develops in cryptogenic cirrhosis, and may represent the most worrisome complication of non-alcoholic steatohepatitis. Non-alcoholic steatohepatitis is tightly related to insulin resistance and several features of the metabolic syndrome, i.e obesity, type 2 diabetes and dyslipidaemia. Nearly two-thirds of adults in the United States and an increasing percentage of the population worldwide are overweight or obese. Diabetes prevalence is increasing as well. The rising prevalence of risk factors associated with non-alcoholic steatohepatitis can partially account for the increasing incidence of cryptogenic cirrhosis and subsequent hepatocellular carcinoma. Moreover, recent evidence demonstrates that both obesity and diabetes are per se associated with an increased cancer risk. Large prospective studies show a significant association with obesity for several cancers, including cancers of the colon, female breast, endometrium, kidney, oesophagus and liver (hepatocellular carcinoma). Type 2 diabetes is also related with increased risks of colon, endometrial, kidney, pancreatic cancer and hepatocellular carcinoma. In western countries, the insulin resistance syndrome is emerging as a risk factor for a wide variety of cancers, including hepatocellular carcinoma.
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PMID:Review article: steatosis, the metabolic syndrome and cancer. 1622 71

Recent evidence indicates that obesity and related metabolic abnormalities are associated with increased incidence or mortality for a number of cancers, including those of the colon, prostate, and pancreas. Obesity, physical inactivity, visceral adiposity, hyperglycemia, and hyperinsulinemia are relatively consistent risk factors for colon cancer and adenoma. Also, patients with type 2 diabetes mellitus have a higher risk of colon cancer. For prostate cancer, the relationship to obesity appears more complex. Obesity seems to contribute to a greater risk of aggressive or fatal prostate cancer but perhaps to a lower risk of nonaggressive prostate cancer. Furthermore, men with type 2 diabetes mellitus are at lower risk of developing prostate cancer. Long-standing type 2 diabetes increases the risk of pancreatic cancer by approximately 50%. Furthermore, over the past 6 years, a large number of cohort studies have reported positive associations between obesity and pancreatic cancer. Together with data from prediagnostic blood specimens showing positive associations between glucose levels and pancreatic cancer up to 25 years later, sufficient evidence now supports a strong role for diabetes and obesity in pancreatic cancer etiology. The mechanisms for these associations, however, remain speculative and deserve further study. Hyperinsulinemia may be important, but the role of oxidative stress initiated by hyperglycemia also deserves further attention.
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PMID:The role of obesity and related metabolic disturbances in cancers of the colon, prostate, and pancreas. 1749 13

The relationship between type 2 diabetes mellitus and pancreatic cancer (PC) is not clear. It has been reported that the increased release of islet amyloid polypeptides (IAPPs) is responsible for the impaired glucose tolerance in PC patients. However, no information exists on the patterns of IAPP expression in PC tissue in comparison with tissue from the normal pancreas and that of a patient with type 2 diabetes. Therefore, we performed a morphometric study and compared the patterns of IAPP expression in 5 normal pancreases (as a control), 6 pancreases from patients with type 2 diabetes, and 11 surgical PC specimens, which were processed for immunohistochemistry using anti-insulin and an anti-IAPP antibody. From the cancer tissue, sections were taken from the tumor (T) and from adjacent tumor-free areas (TF). The size of islets and the number of immunostained cells in these islets were recorded. In diabetes and PC, the size of islets and the number of beta-cells was significantly lower than in the controls. Also, the number of IAPP-expressing cells was significantly lower in diabetes and in the T area but not in the TF region. In addition, no characteristic changes found in diabetic pancreases were observed in the TF area, indicating that PC patients had no prior diabetic diseases. The reduction in the number of IAPP in the T area seems to argue against the role of IAPP in glucose abnormality in PC patients. The primary endocrine alteration in the tumor area suggests that cancer cells produce diabetogenic substances, the nature of which awaits further research.
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PMID:Diabetes mellitus in pancreatic cancer: is it a causal relationship? 1790 50


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