Relevant bibliographies by topics / Non-insulin-dependent diabetes mellitus (NIDDM)

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Non-insulin-dependent diabetes mellitus (NIDDM)'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 April 2022

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Journal articles on the topic "Non-insulin-dependent diabetes mellitus (NIDDM)"

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Nosadini, R., M. R. Cipollina, A. Solini, M. Sambataro, A. Morocutti, A. Doria, P. Fioretto, E. Brocco, B. Muollo, and F. Frigato. "Close relationship between microalbuminuria and insulin resistance in essential hypertension and non-insulin dependent diabetes mellitus." Journal of the American Society of Nephrology 3, no. 4 (October 1992): S56. http://dx.doi.org/10.1681/asn.v34s56.

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The aim of this study was to investigate the relationships among insulin resistance and albumin excretion rate in 25 nondiabetic patients with essential hypertension and in 28 patients with non-insulin dependent diabetes mellitus (NIDDM). Two groups of healthy subjects matched for age, sex, and weight served as controls. Patients with essential hypertension were divided into two subgroups: without (H1) and with (H2) microalbuminuria. Diabetic patients were divided into four subgroups: those with normoalbuminuria without (NIDDM1) and with (NIDDM2) hypertension and those with microalbuminuria without (NIDDM3) and with (NIDDM4) hypertension. Whole-body glucose utilization during euglycemic hyperinsulinemic clamp (40 mU/m2/min insulin infusion) was calculated by tracer dilution techniques (6,6 2H2 glucose tracer continuous infusion) and was significantly lower in hypertensives with microalbuminuria than in those without (H2 versus H1 versus controls: 3.41 +/- 0.51 versus 6.52 +/- 0.62 versus 7.03 +/- 0.48 mg/kg/min; mean +/- SE). Whole-body glucose utilization in NIDDM patients--NIDDM4 versus NIDDM3 versus NIDDM2 versus NIDDM1 versus controls--was: 1.86 +/- 0.31 versus 2.21 +/- 0.39 versus 2.01 +/- 0.40 versus 5.98 +/- 0.77 versus 5.52 +/- 0.92 mg/kg/min (mean +/- SE). Whereas the first three subgroups did not differ among themselves, they had significantly lower glucose utilization than did the normotensive NIDDM1 patients without microalbuminuria and nondiabetic controls (P < 0.01). Hypertensives with microalbuminuria had higher Vmax of sodium-lithium countertransport (Na/Li CTT) in red blood cells than did both hypertensives without microalbuminuria and controls. It was also observed that NIDDM patients with microalbuminuria had higher Vmax of Na/Li CTT than did NIDDM patients without microalbuminuria and controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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Dreval`, A. V. "Treatment of uncomplicated non-insulin-dependent diabetes mellitus (lecture)." Problems of Endocrinology 41, no. 4 (August 15, 1995): 27–34. http://dx.doi.org/10.14341/probl11460.

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Type II diabetes mellitus, or non-insulin-dependent diabetes mellitus (NIDDM) is a common endocrine disease, it affects up to 5-10% of the population aged 60-70 years, the frequency of NIDDM increases rapidly in individuals over 40, although it can occur at an earlier age. Mortality among patients with NIDDM is approximately 2 times higher than among people without diabetes. In particular, in patients with NIDDM under the age of 50 years, life expectancy is reduced by 5-10 years. Moreover, the life expectancy of women is less than that of men, but this difference disappears with age. The main cause of death with NIDDM is cardiovascular and cerebrovascular diseases. However, the prognosis of the disease depends not only on the degree of normalization of metabolism, but also on the effectiveness of the treatment of such often concomitant NIDDM conditions as hypertension, obesity, hyperlipidemia, as well as the elimination of bad habits, in particular smoking.
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Rorsman, P., P.-O. Berggren, K. Bokvist, and S. Efendic. "ATP-Regulated K+ Channels and Diabetes Mellitus." Physiology 5, no. 4 (August 1, 1990): 143–47. http://dx.doi.org/10.1152/physiologyonline.1990.5.4.143.

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Glucose-stimulated insulin secretion from pancreatic Beta-cells is dependent on closure of ATP-regulated K+ channels. These channels are selectively blocked by hypoglycaemic sulfonylureas, compounds used in treatment of non-insulin-dependent diabetes mellitus (NIDDM). This suggests that NIDDM may result from defective K+-channel regulation.
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Jeanrenaud, B., and S. Halimi. "Insulin resistance in non-insulin-dependent diabetes mellitus (NIDDM)." Diabetes Research and Clinical Practice 4 (January 1988): 6–7. http://dx.doi.org/10.1016/0168-8227(88)90004-6.

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Akanuma, Y. "Non-insulin-dependent Diabetes Mellitus (NIDDM) in Japan." Diabetic Medicine 13 (September 1996): 11–12. http://dx.doi.org/10.1002/dme.1996.13.s6.11.

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Min, Hun-Ki. "Non-insulin-dependent Diabetes Mellitus (NIDDM) in Korea." Diabetic Medicine 13 (September 1996): 13–15. http://dx.doi.org/10.1002/dme.1996.13.s6.13.

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Teisberg, Per. "Genetics of non-insulin-dependent diabetes mellitus (NIDDM)." Journal of Internal Medicine 234, no. 5 (November 1993): 439–40. http://dx.doi.org/10.1111/j.1365-2796.1993.tb00774.x.

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Beck-Nielsen, Henning, Jan Erik Henriksen, Allan Vaag, and Ole Hother-Nielsen. "Pathophysiology of non-insulin-dependent diabetes mellitus (NIDDM)." Diabetes Research and Clinical Practice 28 (January 1995): S13—S25. http://dx.doi.org/10.1016/0168-8227(95)01082-o.

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HOBBS, C. G. L., M. KODIKARA, R. GRAY, P. BORDIN, A. ROBINSON, P. J. PACY, S. VENKATESAN, and D. HALLIDAY. "Lipoproteins in non-insulin dependent diabetes mellitus (NIDDM)." Biochemical Society Transactions 24, no. 2 (May 1, 1996): 153S. http://dx.doi.org/10.1042/bst024153s.

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Ekoé, J. M. "Epidemiology of non-insulin-dependent diabetes mellitus (NIDDM)." Diabetes Research and Clinical Practice 4 (January 1988): 66–70. http://dx.doi.org/10.1016/0168-8227(88)90017-4.

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Dissertations / Theses on the topic "Non-insulin-dependent diabetes mellitus (NIDDM)"

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Davoren, Peter M. "The role of non-esterified fatty acids in non-insulin dependent diabetes mellitus." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323655.

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Baroni, Marco Giorgio. "Genetic analysis of non-insulin dependent diabetes mellitus (NIDDM) using DNA markers at candidate gene loci." Thesis, Queen Mary, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294972.

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Cameron-Smith, David, and edu au jillj@deakin edu au mikewood@deakin edu au wildol@deakin edu au kimg@deakin. "THE INTERACTION OF DIETARY FIBRE, CARBOHYDRATE METABOLISM AND DIABETES IN THE RAT." Deakin University. School of Health and Behavioral Sciences, 1994. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20040622.171657.

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It is currently accepted that the most appropriate diet in the treatment of non-insulin-dependent diabetes mellitus "eNIDDM"e is high in carbohydrates, high in fibre and low in fat. Dietary fibre reduces the rate of carbohydrate absorption, which may have a beneficial effect on insulin action. Furthermore, high fibre diets also increase the amount of carbohydrates which are not absorbed from the small intestine. These malabsorbed carbohydrates are fermented by the bacterial population in the large intestine, producing short chain fatty acids "eSCFA"e, including propionate, which has been shown to alter liver carbohydrate metabolism. This thesis investigated the actions of slowed carbohydrate absorption and carbohydrate malabsorption in streptozotocin-induced "eSTZ"e diabetic rats. High carbohydrate diet supplemented with guar gum, a soluble dietary fibre, fed to STZ diabetic rats improved insulin sensitivity. investigation of the alterations in the stomach and small intestine demonstrated that guar increased the viscosity of the meal in the intestine. The action of increased fermentation, producing more propionate, was investigated by supplementing propionate into the diets of STZ diabetic rats or when perfused into isolated rat livers. No changes in insulin action or liver glucose metabolism were measured. in addition, it was shown that guar gum reduces food intake in STZ diabetic rats. Mild reductions in food intake in STZ diabetic rats were shown to increase insulin action. In summary, STZ diabetic rats fed high carbohydrate, high fibre diets reductions in food consumption and slowed carbohydrate absorption are important factors which may lower blood glucose concentrations and increase insulin action. increased SCFA production is unlikely to contribute significantly to the improvements in insulin action.
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McGurk, Colm. "Endothelial function in non-insulin dependent diabetes mellitus." Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387879.

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Alcolado, Juan Carlos. "The genetics of non-insulin dependent diabetes mellitus." Thesis, University of Southampton, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.358901.

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Jaap, Alan James. "Microvascular function in non-insulin-dependent diabetes mellitus." Thesis, University of Glasgow, 1994. http://theses.gla.ac.uk/30732/.

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Epidemiological studies suggest differences in the prevalence and natural history of microvascular complications between subjects with insulin dependent (IDDM) and non-insulin dependent (NIDDM) diabetes. The haemodynamic hypothesis proposes that early functional changes in the microcirculation result in the eventual development of diabetic microangiopathy. There is now a large body of experimental evidence in support of this hypothesis in patients with IDDM, with abnormalities in blood flow, capillary pressure and permeability having been demonstrated. In contrast, there have been few studies investigating microvascular function in NIDDM; however, preliminary work has identified a profound limitation in microvascular vasodilation at an early stage, while capillary pressure does not appear to be elevated. The aim of this thesis was to further investigate functional changes in the skin microcirculation in patients with NIDDM and impaired glucose tolerance (IGT). 1. Using a sensitive plethysmographic system, no difference was found in microvascular fluid permeability between patients with NIDDM and control subjects (5.3 (3.2-9.1) x 10-3 ml.min-1.100g tissue-1.mmHg-1 vs 5.4 (3.5-8.0) x 10-3 ml.min-1. 100g tissue-1 .mmHg-1 median and range; p = 0.98, Mann-Whitney). 2. In confirmation of previous studies, reduced microvascular hyperaemia in response to local heating of the skin was found (using laser Doppler fluximetry) in NIDDM patients with large vessel disease excluded (0.82 (0.42-1.41) V vs 1.40 (0.89-2.13) V control subjects; p < 0.005). Limited vasodilation correlated with fasting plasma insulin (Rg =-0.63, p < 0.04) but not glycaemic control. Microvascular hyperaemia increased after one year of improved glycaemic control in recently diagnosed patients (1.20 (0.51-3.93) V vs 0.97 (0.22-2.17) V at baseline; p < 0.05). In hypertensive NIDDM patients, there was no further reduction in microvascular vasodilation (1.05 (0.70-1.42) V vs 1.04 (0.79-1.63) V normotensive NIDDM, p = 0.82), although there was an increase in calculated resistance to blood flow (127.2 (87.5-181.3) mmHg.V-1 vs 84.7 (61.9-123.0) mmHg.V-1 normotensive patients, p < 0.02). 3. Reduced microvascular hyperaemia was found in subjects with IGT (1.01 (0.71-1.57) V vs 1.41 (1.32-2.13) V control subjects, p < 0.001), and also insulin resistant patients with acromegaly (0.96 (0.56-1.70) V vs 1.46 (1.24-2.13) V control subjects, p < 0,05). In subjects with IGT, limited vasodilation was found to correlate with fasting plasma insulin (Rg = -0.7; p < 0.001) and insulin sensitivity (Rs = 0.52; p < 0.02), but not with β-cell function, plasma glucose or serum lipid concentrations. 4. Using iontophoresis and laser Doppler fluximetry, defective endothelium-dependent vasodilation was found in subjects with IGT (518 (410-905) AU-min-l vs 1236 (875-1588) AU.min-1 control subjects, median and range; p < 0.003). In contrast there was no significant difference in myogenic (683 (301-1175) AU.min-1 vs 898 (303-998) AU.min-1 control subjects; p = 0.5) or neurogenic vasodilation ( 61 (31-109) AU vs 46 (37-146) control subjects; p = 0.8). 5. No differences in skin capillary density were found between patients with NIDDM, subjects with IGT and control subjects under basal conditions (112 (71-144) caps.mm-2 vs 107 (76-140) caps.mm-2 vs 112 (76-138) caps.mm-2 respectively; p= 0.9, Kruskal Wallis), or after venous occlusion (122 (87-157) caps.mm-2 vs 121 (90-143) caps.mm-2 IGT vs 123 (81-147) caps.mm-2; p= 0.9). In light of the above results, a unifying hypothesis has been proposed to explain the differences in epidemiology and pathophysiology of microvascular disease between IDDM and NIDDM.
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Al-Hussary, Nabeel A. J. "Insulin receptor binding in hypertension and non-insulin dependent diabetes mellitus." Thesis, Aston University, 1986. http://publications.aston.ac.uk/14510/.

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Keller, Heather. "The effect of P:S ratio on glycemic control and insulin sensitivity in NIDDM /." Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60533.

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The independent effect of a high polyunsaturated:saturated fat (P:S) diet on glycemic control in humans has been poorly studied. We propose that a P:S $>$ 1.0 vs P:S 1.0 vs. P:S 1.0. HDL and IGFl were significantly lower with the P:S $>$ 1.0. Si was unaffected by the P:S difference, however, trends towards decreased Sg and increased insulin secretion were seen with P:S $>$ 1.0. The small sample size limits the making of firm conclusions, however, it suggests that glycemic control may be improved through increased insulin secretion a result of an increase in P:S.
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Tan, Kathryn Choon Beng. "Postprandial lipoprotein metabolism in non-insulin-dependent diabetes mellitus." Thesis, Cardiff University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323795.

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Whitelaw, Donald C. "Aspects of insulin secretion and action in non-insulin-dependent diabetes mellitus." Thesis, University of Edinburgh, 1999. http://hdl.handle.net/1842/22738.

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In a cross-sectional survey of coronary risk factors in subjects with recently diagnosed NIDDM I confirm the high prevalence of individual risk factors described by others, and show a broadly normal distribution pattern for the clustering of risk factors forming Reaven's Syndrome X, in contrast to that reported in other populations. I suggest that hyperinsulinaemia and hypertriglyceridaemia are the best markers of high coronary risk and note the association of obesity and other risk factors. In a study to examine the effects of the new oral hypoglycaemic drug A4166 in NIDDM I confirm its major effect as an insulin secretagogue but find limited effects on intermediary metabolism when assessed during and intravenous glucose tolerance test. Any enhancement of glucose clearance appears to be secondary to the increase in insulin secretion. If hypertriglyceridaemia exacerbates insulin resistance in NIDDM, then its treatment may reverse this process. In a randomised study comparing the fibrate drug gemfibrozil with placebo I show that reduction in serum triglyceride concentrations with gemfibrozil is associated with improved insulin sensitivity to non-esterified fatty acid (NEFA) and ketone metabolism but not to glucose metabolism, when assessed using a low-dose incremental insulin infusion technique. In established diabetes (NIDDM) the contribution of body fat to insulin resistance is less clear than among non-diabetic subjects. In a group of NIDDM subjects I show no consistent effects of body fat on insulin resistance using the low-dose incremental insulin infusion, and no relation between body fat indices and euglycaemic clamp measures of insulin sensitivity. From the insulin infusion data I show that fasting glucose concentration has the greatest impact on insulin resistance, suggesting that hyperglycaemia or perhaps glucose toxicity has an effect overwhelming that of other factors. Using the data from the body fat studies described, I compare measures of insulin resistance derived from insulin infusions, euglycamic clamps and homeostatic modelling (HOMA-R) in NIDDM, and discuss uses and limitations of these techniques. In a concluding chapter I attempt to summarise the findings from these studies and draw together a discussion of the results obtained in the context of the existing published literature.
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Books on the topic "Non-insulin-dependent diabetes mellitus (NIDDM)"

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Alberti, K. G. M. M. and Mazze R. S, eds. Frontiers of diabetes research: Current trends in non-insulin-dependent diabetes mellitus : proceedings of the Symposium on NIDDM : Research and Clinical Frontiers in Diabetes, New York, 4-7 May 1989. Amsterdam: Excerpta Medica, 1989.

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1931-, Sakamoto N., Alberti, K.G.M.M., and Hotta N, eds. Pathogenesis and treatment of NIDDM and its related problems: Proceedings of the Fourth International Symposium on Treatment of Diabetes Mellitus, Nagoya, 26-23 October 1993. Amsterdam: Elsevier Science, 1994.

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Segura, Ana-Geny. Short-term metabolic effects of increased meal frequency in non-insulin-dependent diabetes mellitus (NIDDM). Ottawa: National Library of Canada, 1993.

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Day, John L. The diabetes handbook: Non-insulin dependent diabetes. Wellingborough: Thornsons in collaboration with the British Diabetic Association, 1986.

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R, Williams D. R., ed. Diabetes mellitus. London: Croom Helm, 1986.

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Farid, Mamdouh Salah. Periodontal disease in non-insulin and insulin dependent diabetes mellitus. Manchester: University of Manchester, 1997.

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Al-Hussary, Nabeel Ahmad Jargees. Insulin receptor binding in hypertension and non-insulin dependent diabetes mellitus. Birmingham: Aston University. Department of Molecular Sciences, 1986.

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Diabetes. Philadelphia, Pa: Hanley & Belfus, 2003.

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Clinician's guide to non-insulin-dependent diabetes mellitus: Pathogenesis and treatment. New York: M. Dekker, 1989.

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English, Patrick. Type 2 Diabetes: Pocketbook. London: Informa Healthcare, 2001.

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Book chapters on the topic "Non-insulin-dependent diabetes mellitus (NIDDM)"

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Kribben, A., U. Heemann, and Th Philipp. "Antihypertensive treatment in non-insulin-dependent diabetes mellitus (NIDDM)." In Pharmacology of Diabetes, edited by C. E. Mogensen and E. Standl, 247–62. Berlin, Boston: De Gruyter, 1990. http://dx.doi.org/10.1515/9783110850321-019.

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Permutt, M. Alan, Laszlo Koranyi, and Akira Matsutani. "Molecular Genetic Approach to Polygenic Disease: Non-Insulin Dependent Diabetes Mellitus (NIDDM)." In DNA Polymorphisms as Disease Markers, 43–59. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3690-1_5.

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Lane, Pascale H., S. Michael Mauer, and Michael W. Steffes. "Renal Pathology in Insulin Dependent (IDDM) and Noninsulin Dependent Diabetes Mellitus (NIDDM)." In Nephrology, 1342–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-662-35158-1_137.

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Li, S., and D. J. Galton. "DNA Polymorphisms of the Glucose Transporter Gene in Non-Insulin Dependent Diabetes Mellitus (NIDDM)." In Human Apolipoprotein Mutants 2, 211–14. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4615-9549-6_26.

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Johansen, Klaus, and Sam Dagogo-Jack. "Non-Insulin-Dependent Diabetes Mellitus." In Diabetes Guide, 79–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76868-2_8.

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Tiro, Jasmin, Simon J. Craddock Lee, Steven E. Lipshultz, Tracie L. Miller, James D. Wilkinson, Miriam A. Mestre, Barbara Resnick, et al. "Non-insulin-Dependent Diabetes Mellitus." In Encyclopedia of Behavioral Medicine, 1342. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_101158.

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Gentile, L., S. Turco, E. Rossi, and R. Torella. "Non-Insulin-Dependent Diabetes mellitus and Liver Cirrhosis." In Frontiers in Diabetes, 168–71. Basel: KARGER, 1998. http://dx.doi.org/10.1159/000060908.

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Bennett, Peter H., Clifton Bogardus, William C. Knowler, and Stephen Lillioja. "Antecedent Events for Non-Insulin Dependent Diabetes Mellitus." In Prediabetes, 185–92. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5616-5_22.

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Schmitz, Anita. "Microalbuminuria and Mortality in Non-Insulin-Dependent Diabetes." In The Kidney and Hypertension in Diabetes Mellitus, 65–70. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-1974-1_9.

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Duckworth, William C. "Pathogenesis and Management of Non-Insulin-Dependent Diabetes Mellitus." In Endocrine Function and Aging, 35–47. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3240-7_4.

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Conference papers on the topic "Non-insulin-dependent diabetes mellitus (NIDDM)"

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HU, HAIYAN, and XIAOMAN LI. "NETWORKING PATHWAYS UNVEILS ASSOCIATION BETWEEN OBESITY AND NON-INSULIN DEPENDENT DIABETES MELLITUS." In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 2007. http://dx.doi.org/10.1142/9789812776136_0026.

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Alava, I., L. J. Garcia Frade, H. de la Calle, J. L. Havarro, L. J. Creighton, and P. J. Gaffney. "DIABETES MELLITUS: HYPERCOAGULABILITY AID HYPOFIBRIHOLYSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643108.

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A hypercoagulable state has been related to the presence of microvascular and macrovascular disease in Diabetes Mellitus. The aim of this study was to establish when this hypercoagulable state appears and the response of the fibrinolytic system.43 patients (29 males, 14 females, aged 19-73), 28 insulin-dependent (10 of them with micro and/or macrovascular disease), 15 non insulin- dependent (all of them with vascular disease) were studied.Platelet aggregation and adenine nucleotides, plasma and serum thromboxane B2 (TxB2), Factor VIII Coagulant (VIII-C), Factor VIII Related antigen (VIII-RAg), Factor VIII Ristocetin Cofactor (VIII-RCoF), Fibronectin, Tissue Plasminogen Activator (t-PA) and X-Oligomers fibrin fragments were measured.In the diabetic patients maximal aggregation was induced by a threshold concentration of adenosin diphosphate and arachidonic acid lower than in controls (p<0.01 and p<0.05). Diabetic patients also presented elevated platelet ADP and decreased platelet c-AMP. They had higher plasma TxB* levels than the control group.FVIII-C, FVIII-RAg and Fibronectin were increased (p<0.001) both in patients type I and II, with and without vasculopathy. FVIII-RCoF was highly increased in vasculopathy (p<0.001) while was non significant without it.The patients with vasculopathy presented decreased t-PA plasma levels (p<0.05). lo difference in X-Oligomers was found related to controls.These findings suggest: 1) A hypercoagulable state previously to the development of clinical vasculopathy. 2) A decreased fibrinolytic response associated to vasculopathy.
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Woo, D. G., Q. J. Lee, W. P. Park, C. Y. Ko, D. Lim, H. S. Kim, and B. Y. Lee. "Relationship Between Obesity and Osteopenia in Lumbar Spines of Rats Using Mechanical and Morphological Studies." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192537.

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Obesity (OB) and osteopenia (OP), grave consequences for human health, quality of life, and even the efficiency of the labor force and economy, are two common complex diseases. Two public health problems have exploded in prevalence over the past decade [1]. OB, now a major epidemic in the developed world and frequent among elderly subjects, is a condition of excessive body fat that causes or exacerbates several risk of developing non-insulin dependent diabetes mellitus, cardiovascular disease, cancer and other diseases [2]. OP is defined as a systemic skeletal disease caused by low bone mass and microstructural deterioration of the bone.
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Yulianti, Kartika, Aris Wibudi, and Mila Citrawati. "Relation Between Tiroid Status with Glycemic Control of Type 2 DM Patients at RSPAD Gatot Soebroto." In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.05.12.

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ABSTRACT Background: Diabetes Mellitus (DM) is a group of symptoms that arise due to increased blood sugar levels. Diabetes Mellitus type 2 has a higher risk of developing thyroid dysfunction. Thyroid dysfunction can affect various body metabolism and result in insulin resistance, significantly affecting glycemic control in DM patients. This study aimed to determine the relation between thyroid status as assessed by the level of thyroid-stimulating hormone (TSH), free thyroxine (FT4), and glycemic control (HbA1c). Subjects and Method: A cross-sectional study. A sample of 38 DM patients was selected by purposive sampling. The dependent variable was glycemic control. The independent variables were TSH and FT4. Patients were classified into 4 quartiles (Q) based on their TSH and FT4 levels. Statistic test used was non parametric for category group of variables, which was Chi square test. Results: Mean of fasting blood glucose was 200,56 mg/dL (modus 137 mg/dL), mean of 2 hours post prandial blood glucose was 247 mg/dL (modus 305 mg/dL). Subjetcs with poor glycemic control dominated as much as 76%. Most subjects had TSH level at Q4 (36%), while most of the subjects had FT4 level at Q1 (34%). The results showed that 38 samples with poor glycemic control were 72% in the 4th quartile (Q4) (> 3.1750 mU / L) TSH, and 64.7% were in Q1 (≤ 11.8400) FT4. The analysis showed that there was a significant relation between TSH (p = 0.047) and FT4 (p = 0.041) with glycemic control in type 2 DM patients. Conclusion: FT4 and TSH levels relate to glycemic control in type 2 DM patients Keywords: TSH, FT4, HbA1c, Diabetes Mellitus Correspondence: Mila Citrawati. Department of Faal, Faculty of Medicine, UPN Veteran, Jakarta. Jl. RS Fatmawati, Pondok Labu, South Jakarta 12450, Telp. (021) 7656971. E-mail: milacitrawati@upnvj.ac.id. Mobile: 081282990515 DOI: https://doi.org/10.26911/the7thicph.05.12
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Mombaerta, P., V. Ballegeer, P. Declerck, F. A. Van Assche, and D. Collen. "FIBRINOLYTIC RESPONSE TO VENOUS OCCLUSION, AND FIBRIN FRAGMENT D-DIMER AND FIBRONECTIN LEVELS IN NORMAL AND COMPLICATED PREGNANCY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643143.

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The fibrinolytic response to venous occlusion was assessed in pregnant women with measurements of total and free t-PA, using specific ELISAs based on monoclonal antibodies.Total t-PA levels increased after venous occlusion with 11±8 ng/ml (mean ± SD) in healthy fertile non-pregnant women (n=6), with 0.8 ± 1.3 ng/ml in 2nd trim. (n=5) and with 3.8 ± 3.9 ng/ml in 3rd trim. (n=4) healthy pregnant women. The increase in free t-PA was 12 ± 11; 1.2 ± 0.9 and 0 ng/ml respectively. The difference in post- and pre-occlusion levels in 3rd trim, pregnant women with insulin dependent diabetes mellitus IDDM (n=4) was 3.2 ± 4.2 ng/ml, with intrauterine growth retardation (IUGR) (n=4) 2.6 ± 3.0 ng/ml and with preeclampsia (n=5) 3.2 ± 3.5 ng/ml for total t-PA and 0, 0 and 0 ng/ml for free t-PA.Fibrin fragment D-dimer levels in plasma measured with a specific ELISA were 130 ± 36 ng/ml in healthy fertile non-pregnant women (n=8). A significant increase was found in 4 out of 5 1st trim., 25 out of 25 2nd trim, and 21 out of 22 3rd trim, normal pregnant women. In these groups, plasma levels were 340 ± 160, 400 ± 170 and 440 ± 220 ng/ml respectively.Fibronectin levels, measured with a Laurell electroimmunoassay and expressed as percentage of pooled human plasma (=330 yg/ml) were 83 ± 26% in 2nd trim, patients (n=24) and 102 ± 35% in 3rd trim, patients (n=17). Normal fibronectin levels were found in 4 patients with IDDM and in 6 with IUGR, whereas in 6 out of 8 preeclamptic patients significantly increased levels were observed.These results confirm, with the use of a newly developed free t-PA assay, that the fibrinolytic response to venous occlusion is completely inhibited in the 3rd trimester of pregnancy. A reduced release of t-PA from the vessel wall during venous occlusion and/or an increased inhibition of released t-PA were observed. No difference was found in the fibrinolytic response between normal and complicated pregnancy. D-dimer levels are significantly elevated during pregnancy. Finally, the usefulness of fibronectin for the diagnosis of preeclampsia is confirmed.
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