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)

This case report shares our experience using the transtheoretical model of health behavior change to promote exercise in a type 2 diabetes patient. The patient was under our care from May through July 2006, during which time the patient was under regular observation and interviewed to collect data. A total of two outpatient consultations and five telephone interviews were conducted. An analysis of results showed the subject to be in the preparation stage of behavior change. To help move the subject into the action stage, the author promoted regular exercise through a variety of strategies, including self-reevaluation, self-change plan development, self-liberation, contingency management, social support search and environmental reevaluation. After nursing intervention, the subject maintained an exercise journal and arranged his own exercise plan. His exercise regimen gradually increased the frequency and intensity of exercise and further extended the scope of exercise to include regular exercise with family members. The author hopes that this case report may provide a reference for health professionals on the use of the transtheoretical model of health behavior change in the care of this type of patient.
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PMID:[An experience using the transtheoretical model of health behavior change to promote exercise in a type 2 diabetes patient]. 1793 53

The prostaglandin E synthase 2 (PTGES2) gene maps to a locus linked to obesity and is involved in the synthesis of the antilipolytic compound prostaglandin E(2). In a recent study, we found an association of the minor PTGES2 Arg298His allele and lower risk of type 2 diabetes mellitus in the European Investigation into Cancer and Nutrition (EPIC) and Cooperative Health Research in the Augsburg Region (KORA) cohorts. Here, we employed our Metabolic Intervention Cohort Kiel (MICK) to assess the influence of the PTGES2 Arg298His polymorphism on a wider scale of parameters of the metabolic syndrome and postprandial metabolism. In comparison to subjects homozygous for the Arg allele, carriers of the His-allele showed significantly lower fasting insulin (geometric mean +/- SEM: 11.8 muU/mL, 11.41-12.25 versus 13.0, 12.71-13.33; p = 0.023), lower postprandial insulin levels after an oral glucose tolerance test (area under the curve 77.2, 74.07-80.52 versus 81.2, 78.8-83.63; p = 0.023) and lower homeostasis model assessment (HOMA)-insulin-resistance (3.030, 2.909-3.157 versus 3.346, 3.257-3.438; p = 0.041) and HOMA-beta-cell-function (107.2, 104.04-110.52 versus 117.2, 114.65-119.71; p = 0.019). Adjustment for body mass index (BMI) resulted in a loss of these significant differences. BMI tended to show lower values in His-allele carriers, (p = 0.067). In conclusion, risk-reducing effects of the minor His allele of the PTGES2 Arg298His polymorphism could be mediated partly by lowered BMI.
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PMID:Prostaglandin E synthase 2 (PTGES2) Arg298His polymorphism and parameters of the metabolic syndrome. 1797 97

Protein phosphorylation represents one of the key regulatory events in physiological insulin secretion from the islet beta-cell. In this context, several classes of protein kinases (e.g. calcium-, cyclic nucleotide- and phospholipid-dependent protein kinases and tyrosine kinases) have been characterized in the beta-cell. The majority of phosphorylated amino acids identified include phosphoserine, phosphothreonine and phosphotyrosine. Protein histidine phosphorylation has been implicated in the prokaryotic and eukaryotic cellular signal transduction. Most notably, phoshohistidine accounts for 6% of total protein phosphorylation in eukaryotes, which makes it nearly 100-fold more abundant than phosphotyrosine, but less abundant than phosphoserine and phosphothreonine. However, very little is known about the number of proteins with phosphohistidines, since they are highly labile and are rapidly lost during phosphoamino acid identification under standard experimental conditions. The overall objectives of this review are to: (i) summarize the existing evidence indicating the subcellular distribution and characterization of various histidine kinases in the islet beta-cell, (ii) describe evidence for functional regulation of these kinases by agonists of insulin secretion, (iii) present a working model to implicate novel regulatory roles for histidine kinases in the receptor-independent activation, by glucose, of G-proteins endogenous to the beta-cell, (iv) summarize evidence supporting the localization of protein histidine phosphatases in the islet beta-cell and (v) highlight experimental evidence suggesting potential defects in the histidine kinase signalling cascade in islets derived from the Goto-Kakizaki (GK) rat, a model for type 2 diabetes. Potential avenues for future research to further decipher regulatory roles for protein histidine phosphorylation in physiological insulin secretion are also discussed.
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PMID:Emerging roles for protein histidine phosphorylation in cellular signal transduction: lessons from the islet beta-cell. 1840 53

PLD's (Phospholipases D) are ubiquitously expressed proteins involved in many transphosphatidylation reactions. They have a bi-lobed structure composed by two similar domains which at their interface reconstitute the catalytic site through the association of the two conserved HxKx(4)Dx(6)GSxN motifs. PLD1 interacts with the small phosphoprotein PED-PEA15 by an unknown mechanism that, by enhancing PLD1 stability, apparently increases its enzymatic activity; the minimum interacting region of PLD1 was previously identified as spanning residues 712-1074 (D4 region). Since the D4/PED-PEA15 interaction has been claimed to be one of the multiple molecular events that can trigger type 2 diabetes, we purified the two recombinant proteins to study in vitro this binding by both ELISA and SPR techniques. Whilst PED-PEA15 was easily expressed and purified, expression of recombinant D4 was more problematic and only the fusion protein with Thioredoxin A and a six Histidine Tag (Trx-His(6)-D4) demonstrated sufficient stability for further characterization. We have found that Trx-His(6)-D4 is present as two different oligomeric forms, though only the monomeric variant is able to interact with PED-PEA15. All these findings may have important implications for both the mechanisms of phospholipase activity and PED-PEA15 regulative functions.
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PMID:Expression and purification of the D4 region of PLD1 and characterization of its interaction with PED-PEA15. 1842 Apr 20

A 77-year-old Japanese man was admitted due to hypoglycemia induced by small amount of insulin. He was diagnosed type 2 diabetes in 1978 and the pancreatic cancer in 1993. Resection of the pancreas head and duodenum was performed. Subsequently, anastomotic stenosis appeared to induce appetite loss. His flavor for carbohydrate-rich food accelerated protein malnutrition. Fatty liver and pancreas atrophy were diagnosed in 1999. After he was diagnosed as secondary kwashiorkor, nasal feeding of protein-rich food improved his fatty liver as well as his general condition rapidly. Anastomotic stenosis and pancreas atrophy contributed to a combination of type 2 diabetes and kwashiorkor.
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PMID:Combination of type 2 diabetes and malnutrition worsened by anastomotic stenosis and pancreas atrophy following resection of pancreas head. 1859 45

We present the previously unreported hazard of creating pressure ulceration in a susceptible host by the improper use of a silicone prosthetic liner. An 80-yr-old man sustained a recent transtibial amputation for peripheral vascular disease. His comorbidities included vascular cognitive impairment, type 2 diabetes mellitus, coronary artery disease, anemia of chronic disease, postherpetic neuralgia, and pruritus of uncertain origin. When not using his transtibial prosthesis, he found his 1.5-mm thick silicone liner (ICEROSS) more comfortable to wear than his stump shrinker and thermoplastic protector. Moreover, he repeatedly wore his liner rolled partway down his stump to allow him to scratch pruritic skin. A horizontal, linear, stage 2 ulcer developed on the residual limb under the upper edge of the rolled liner. The ulcer required >3 mos to heal. This case illustrates the importance of candidate selection for roll-on liners, proper patient and professional training, and optimal management of patient comorbidities.
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PMID:Improper use of a transtibial prosthesis silicone liner causing pressure ulceration. 1897 72

We present a case of a 40-year-old man with strong family history of diabetes. His pancreatic ultrasonography was normal at the discovery of his diabetes. Anti-pancreatic antibodies were negative. The patient was treated by insulin and continued to loose weight. His diabetes remained unstable during the follow-up. Three years later, a pancreatic adenocarcinoma was diagnosed which was locally advanced and could not be removed surgically. This observation argues among several mechanisms explaining diabetes in subjects with pancreatic cancer, in favor of tumor-derived diabetogenic substance and suggests that diabetes mellitus could reveal pancreatic cancer even in the presence of conventional risk factors of type 2 diabetes.
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PMID:Diabetes mellitus as an early symptom of pancreatic cancer diagnosed three years later. 1899 44

Islet amyloid polypeptide (IAPP), a 37-amino acid polypeptide hormone of the calcitonin family, is colocalized and cosecreted with insulin in secretory granules of pancreatic islet beta cells. IAPP can assemble into toxic oligomers and amyloid fibrils, a hallmark of type 2 diabetes. Its interactions with insulin in the secretory granules might influence the formation of cytotoxic oligomers and amyloid fibrils. Presented NMR analysis shows that IAPP, free in solution and in complex with insulin, retains elements of residual secondary structure. NMR chemical shifts and (15)N relaxation data as well as 49 ns replica exchange molecular dynamic simulations indicate that the transiently populated helical structure in residues 11-18 is essential for interactions with insulin. These interactions are mediated by salt bridges between positively charged residues Arg11 or Arg18 of rat IAPP and Glu13 of insulin B chain as well as by hydrophobic interactions flanking the salt bridges. The insulin binding region is composed of the same amino acids in amyloidogenic human IAPP and soluble rat IAPP (with the sole exception of His/Arg-18), implying the same binding mode for both hormones. This His/Arg-18 mutation results in reduced affinity binding of human IAPP to insulin in comparison to rat IAPP as it is detected by surface plasmon resonance biosensor analysis. Implications of the described interactions between soluble forms of IAPP and insulin in preventing oligomerization of human IAPP are discussed.
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PMID:Residual structure in islet amyloid polypeptide mediates its interactions with soluble insulin. 1914 26

In this study we tested whether the type 2 diabetes mellitus associated prostaglandin E synthase 2 arginine to histidine polymorphism at position 298 (R298H) influences prostaglandin E2 levels in humans. Fasting prostaglandin E2 was determined in the blood of subjects carrying different genotypes of the R298H polymorphism. Subjects were matched by sex, age, and body mass index. No differences in prostaglandin E2 levels were found with respect to genotypes when considering the whole group. Male homozygous histidine carriers showed elevated prostaglandin E2 levels compared to heterozygous carriers and homozygous arginine carriers (188.2+/-42.4 vs. 80.4+/-26.5pg/ml, p=0.021; and vs. 92.9+/-15.3pg/ml, p=0.11). These differences were not evident in female subjects. In contrast, 6-keto-prostaglandin F1alpha levels as independent marker of arachidonic acid metabolism showed ambiguous results. Nevertheless, preliminary evidence of the prostaglandin E synthase 2 R298H polymorphism possibly influencing prostaglandin E2 blood levels in a gender-specific manner was obtained.
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PMID:Influence of a type 2 diabetes associated prostaglandin E synthase 2 polymorphism on blood prostaglandin E2 levels. 1926 62

A 63-year-old white man is seen for a routine examination. His medical history is significant for type 2 diabetes mellitus of 16 years duration, diabetic peripheral sensory neuropathy, hypertension, and hyperlipidemia. He smoked 1 pack of cigarettes daily for 20 years but quit many years ago. Salient findings on physical examination include decreased light touch and vibratory sense in the feet, decreased pedal pulses, and hyperpigmented patches on the lower legs. The patches have normal sensation and a hint of atrophy. There is no overlying scale. What is your diagnosis?
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PMID:Puzzles in practice. Diabetic dermopathy. 1949 55


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