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

Until recently, there was little empirical data regarding the psychological impact of screening for type 2 diabetes. There is now some progress in this area, as evidenced by emerging population based studies reporting on the effects of screening for type 2 diabetes on perceived health status and well-being. Recent studies from our own and other groups show that the diagnosis type 2 diabetes has no substantial adverse or positive effect on the participants' perceived health status and well-being after notification of the test result. Importantly, screening-detected type 2 diabetes patients beforehand perceive their risk for type 2 diabetes to be low, despite the presence of risk factors, such as obesity, hypertension and a family history, and overall report low levels of diabetes-related symptom distress. Yet, screening-detected type 2 diabetes patients were bothered more by symptoms of hyperglycaemia and fatigue in the first year following diagnosis type 2 diabetes than non-diabetics. On the basis of research to date, we conclude that screening for type 2 diabetes in the general population has no serious psychological side effects. Whether lack of emotional response to screening, is because of unawareness or indifference, needs further investigation. Future studies should be aiming towards a better understanding of how to raise the awareness and understanding of type 2 diabetes and its risk factors in high-risk individuals, while avoiding or minimizing negative effects, such as emotional distress and denial. The growing number of younger people developing type 2 diabetes warrants further research into labeling effects of an early diagnosis.
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PMID:The psychological impact of screening for type 2 diabetes. 1614 14

To evaluate efficacy and tolerability of telmisartan, an angiotensim II receptor blocker, in reducing microalbuminuria in adult Indian hypertensive patients with type 2 diabetes mellitus, a prospective, open-label, non-comparative, assessor-blind, multicentric, pilot study was conducted in 60 eligible hypertensive patients with type 2 diabetes mellitus and microalbuminuria after obtaining their informed consent. The study was approved by the respective institutional review boards. Each patient received telmisartan 40 mg initially once daily for first 4 weeks which was titrated upwards to 80 mg once daily for the next 8 weeks. Blood pressure was assessed at the end of every 2 weeks and urinary albumin excretion and creatinine clearance were measured at baseline and after 12 weeks of therapy. Safety outcome measures included monitoring of physical examination, laboratory parameters and monitoring treatment-emergent adverse events. Fifty-five patients completed the study while 5 cases were lost to follow-up. The mean age of the patients was 48.27 years. Of the total patients 63.6% were males and 46.4% were females. At baseline the mean urinary albumin excretion rate was 131.81 +/- 38.82 mg/minute. A statistically significant (p < 0.05) reduction (32.96%) in urinary albumin excretion rate occurred after 12 weeks of therapy (118.36 +/- 37.22). The mean pre-study systolic blood pressure was 165.05 +/- 15.24 mmHg which was significantly (p < 0.05) reduced to 123.72 +/- 5.88 mmHg at the end of 12 weeks. At baseline the mean diastolic blood pressure was 103.55 +/- 9.84 mmHg which was significantly (p < 0.05) reduced to 84.71 +/- 8.54 mmHg. The JNC-VII goal of blood pressure below 130/80 was achieved in 34 (61.8%)of the 55 patients at the end of 12 weeks. Both fasting and postprandial blood sugar levels were well-controlled at the end of the study. Telmisartan was well tolerated with only 9.09% of the patients reported mild and transient adverse events like fatigue, dizziness, nausea and diarrhoea. No abnormalities were detected in the laboratory parameters. The results of this pilot study indicate that telmisartan is effective, safe and well tolerated while reducing microalbuminuria in adult Indian hypertensive patients with type 2 diabetes mellitus.
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PMID:A pilot study for evaluation of the efficacy and safety of telmisartan in reducing microalbuminuria in hypertensive patients with type 2 diabetes mellitus. 1617 97

Glycogen phosphorylase inhibition represents a promising strategy to suppress inappropriate hepatic glucose output, while muscle glycogen is a major source of fuel during contraction. Glycogen phosphorylase inhibitors (GPi) currently being investigated for the treatment of type 2 diabetes do not demonstrate hepatic versus muscle glycogen phosphorylase isoform selectivity and may therefore impair patient aerobic exercise capabilities. Skeletal muscle energy metabolism and function are not impaired by GPi during high-intensity contraction in rat skeletal muscle; however, it is unknown whether glycogen phosphorylase inhibitors would impair function during prolonged lower-intensity contraction. Utilizing a novel red cell-perfused rodent gastrocnemius-plantaris-soleus system, muscle was pretreated for 60 min with either 3 micromol/l free drug GPi (n=8) or vehicle control (n=7). During 60 min of aerobic contraction, GPi treatment resulted in approximately 35% greater fatigue. Muscle glycogen phosphorylase a form (P<0.01) and maximal activity (P<0.01) were reduced in the GPi group, and postcontraction glycogen (121.8 +/- 16.1 vs. 168.3 +/- 8.5 mmol/kg dry muscle, P<0.05) was greater. Furthermore, lower muscle lactate efflux and glucose uptake (P<0.01), yet higher muscle Vo(2), support the conclusion that carbohydrate utilization was impaired during contraction. Our data provide new confirmation that muscle glycogen plays an essential role during submaximal contraction. Given the critical role of exercise prescription in the treatment of type 2 diabetes, it will be important to monitor endurance capacity during the clinical evaluation of nonselective GPi. Alternatively, greater effort should be devoted toward the discovery of hepatic-selective GPi, hepatic-specific drug delivery strategies, and/or alternative strategies for controlling excess hepatic glucose production in type 2 diabetes.
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PMID:The experimental type 2 diabetes therapy glycogen phosphorylase inhibition can impair aerobic muscle function during prolonged contraction. 1673 53

Metabolically healthy skeletal muscle possesses the ability to switch easily between glucose and fat oxidation in response to homeostatic signals. In type 2 diabetes mellitus and obesity, the skeletal muscle shows a great reduction in this metabolic flexibility. A substrate like dodecanedioic acid (C-12), able to increase skeletal muscle glycogen stores via succinyl-CoA formation, might both postpone the fatigue and increase fatty acid utilization, since it does not affect insulin secretion. In healthy volunteers and in type 2 diabetic subjects, the effect of an oral C-12 load was compared with a glucose or water load during prolonged, moderate-intensity, physical exercise. C-12 metabolism was analyzed by a mathematical model. After C-12, diabetics were able to complete the 2 h of exercise. Nonesterified fatty acids increased both during and after the exercise in the C-12 session. C-12 oxidation provided 14% of total energy expenditure, and the sum of C-12 plus lipids oxidized after the C-12 meal was significantly greater than lipids oxidized after the glucose meal (P < 0.025). The fraction of C-12 that entered the central compartment was 47% of that ingested. During the first phase of the exercise ( approximately 60 min), the mean C-12 clearance from the central compartment toward tissues was 2.57 and 1.30 l/min during the second phase of the exercise. In conclusion, C-12 seems to be a suitable energy substrate during exercise, since it reduces muscle fatigue, is rapidly oxidized, and does not stimulate insulin secretion, which implies that lipolysis is not inhibited as reported after glucose ingestion.
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PMID:Dodecanedioic acid overcomes metabolic inflexibility in type 2 diabetic subjects. 1678 59

Telomeres are the repeat DNA sequences at the end of chromosomes necessary for successful DNA replication and chromosomal integrity. Telomeres shorten at cell division at a rate determined by oxidative DNA damage, and cells are triggered into replicative senescence once telomeres shorten to a critical length. Telomere-related chromosomal maintenance also has a role in carcinogenesis. Type 2 diabetes is characterised by increased oxidative stress, increased oxidative DNA damage, senescent retinal and renal phenotypes, and an increased risk of epithelial malignancy. We suggest that increased oxidative DNA damage and telomere attrition in type 2 diabetes leads to: (1) carcinogenic telomere-dependent chromosomal non-reciprocal translocations, genomic instability, and the development of epithelial cancers; (2) senescent retinal and renal phenotypes (expressed as diabetic retinopathy and nephropathy); and (3) senescent vascular endothelial, monocyte-macrophage and vascular smooth muscle cells (expressed as endothelial dysfunction and accelerated atherogenesis). An adverse intrauterine environment leads to increased feto-placental oxidative stress and feto-placental oxidative DNA damage. We also suggest that intrauterine oxidative DNA damage and telomere shortening is another point at which increased oxidative stress could contribute to a pre-programmed increased risk of senescent phenotypes in adult offspring, characterised by type 2 diabetes and epithelial malignancy. These suggestions can be used to understand early glucose intolerance in the young children of type 1 diabetes pregnancies, poor cancer outcomes in type 2 diabetes, beta cell fatigue in type 2 diabetes and the absence of increased epithelial cancer risk in type 1 diabetes.
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PMID:Chromosomal telomere attrition as a mechanism for the increased risk of epithelial cancers and senescent phenotypes in type 2 diabetes. 1679 17

Menopause is one of the critical periods of a woman's life during which weight gain and onset or worsening of obesity are favoured. It is at this period when obesity prevalence is the highest. There are several causes for this disorder, ones clearly related with hypo-oestrogenism and others depend on age favouring increased food intake and decreased energy waste. This weight gain is related to adverse health effects that get worse due to changes in fat distribution observed during menopause. The increase in visceral fat favours the development of insulin resistance and its clinical consequences such as carbohydrate metabolism impairments and type 2 diabetes, arterial hypertension, and dyslipidaemia, leading to increased cardiovascular risk, among other complications.
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PMID:[Obesity and menopause]. 1714 59

Metabolic syndrome consists of a cluster of metabolic conditions, such as hypertriglyceridemia, hyper-low-density lipoproteins, hypo-high-density lipoproteins, insulin resistance, abnormal glucose tolerance and hypertension, that-in combination with genetic susceptibility and abdominal obesity-are risk factors for type 2 diabetes, vascular inflammation, atherosclerosis, and renal, liver and heart disease. One of the defects in metabolic syndrome and its associated diseases is excess cellular oxidative stress (mediated by reactive oxygen and nitrogen species, ROS/RNS) and oxidative damage to mitochondrial components, resulting in reduced efficiency of the electron transport chain. Recent evidence indicates that reduced mitochondrial function caused by ROS/RNS membrane oxidation is related to fatigue, a common complaint of MS patients. Lipid replacement therapy (LRT) administered as a nutritional supplement with antioxidants can prevent excess oxidative membrane damage, restore mitochondrial and other cellular membrane functions and reduce fatigue. Recent clinical trials have shown the benefit of LRT plus antioxidants in restoring mitochondrial electron transport function and reducing moderate to severe chronic fatigue. Thus LRT plus antioxidant supplements should be considered for metabolic syndrome patients who suffer to various degrees from fatigue.
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PMID:Metabolic syndrome and mitochondrial function: molecular replacement and antioxidant supplements to prevent membrane peroxidation and restore mitochondrial function. 1724 17

Nutrient overload induces obesity, a primary risk factor for type 2 diabetes. Ribosomal biogenesis and protein synthesis, which are controlled by the mammalian target of rapamycin (mTOR), are primary energy-consuming processes in cells. mTOR phosphorylates and inactivates members of the eukaryotic translation initiation factor 4E-binding (eIF4E-binding) protein (4E-BP) family, which are translational repressors of 5' cap-dependent protein synthesis. In this issue of the JCI, Le Bacquer et al. report that simultaneous deletion of both 4E-BP1 and 4E-BP2 in mice results in insulin resistance, decreased energy expenditure, and increased adipogenesis (see the related article beginning on page 387). These findings link protein synthesis, insulin sensitivity, and body weight.
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PMID:A link between protein translation and body weight. 1727 56

The aim of this study was to design a culturally adapted questionnaire for studying quality of life (QOL) among type 1 and 2 adult diabetes patients in the Islamic Republic of Iran. The 41 items on the questionnaire were based on qualitative research and covered general and health-related QOL. In a descriptive survey, 104 patients completed the questionnaire; 68 (65.4%) were female. Mean age was 50.5 years (standard deviation 12.8). Most patients (86.5%) had type 2 diabetes. Cronbach's alpha coefficient for the questionnaire was 0.98. The questionnaire successfully distinguished the lower QOL of patients suffering from pain in the limbs, loss of appetite, fatigue, constipation and itching. The questionnaire could determine both general and health-related QOL.
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PMID:Developing a culturally valid and reliable quality of life questionnaire for diabetes mellitus. 1754 20

Hypogonadism in men has a complex and varied pathogenesis. In addition to multiple established causes of the disease, low testosterone levels are associated with various comorbidities, including metabolic syndrome and type 2 diabetes. Symptoms associated with hypogonadism include reduced sex drive, fatigue, and mood disturbances, but accurate diagnosis requires biochemical testing. Total testosterone is considered the appropriate testosterone measurement in most situations in primary care, although free testosterone is a more accurate marker and is indicated in some situations. Testosterone replacement therapy is a valid treatment option for men with testosterone deficiency accompanied by symptoms of hypogonadism. The goals of therapy are to restore physiologic testosterone levels and alleviate symptoms. A potential association of testosterone replacement therapy with prostate cancer is the biggest safety concern, so patient monitoring should include regular digital rectal examination and prostate-specific antigen tests.
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PMID:Evolving issues in male hypogonadism: evaluation, management, and related comorbidities. 1754 24


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