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

Economic growth has been the single biggest contributor to population health since the Industrial Revolution. The growth paradigm, by definition, is dynamic, implying similar diminishing returns on investment at both the macro- and the micro-economic levels. Changes in patterns of health in developing countries, from predominantly microbial-related infectious diseases to lifestyle-related chronic diseases (e.g., obesity, type 2 diabetes) beyond a point of economic growth described as the epidemiologic transition, suggest the start of certain declining benefits from further investment in the growth model. These changes are reflected in slowing improvements in some health indices (e.g., mortality, infant mortality) and deterioration in others (e.g., disability-associated life years, obesity, chronic diseases). Adverse environmental consequences, such as climate change from economic development, are also related to disease outcomes through the development of inflammatory processes due to an immune reaction to new environmental and lifestyle-related inducers. Both increases in chronic disease and climate change can be seen as growth problems with a similar economic cause and potential economic and public health-rather than personal health-solutions. Some common approaches for dealing with both are discussed, with a plea for greater involvement by health scientists in the economic and environmental debates in order to deal effectively with issues like obesity and chronic disease.
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PMID:Health, "illth," and economic growth: medicine, environment, and economics at the crossroads. 1952 47

Although the human genome has remained unchanged over the last 10,000 years, our lifestyle has become progressively more divergent from those of our ancient ancestors. This maladaptive change became apparent with the Industrial Revolution and has been accelerating in recent decades. Socially, we are people of the 21st century, but genetically we remain similar to our early ancestors. In conjunction with this discordance between our ancient, genetically-determined biology and the nutritional, cultural and activity patterns in contemporary Western populations, many diseases have emerged. Only a century ago infectious disease was a major cause of mortality, whereas today non-infectious chronic diseases are the greatest cause of death in the world. Epidemics of metabolic diseases (e.g., cardiovascular diseases, type 2 diabetes, obesity, metabolic syndrome and certain cancers) have become major contributors to the burden of poor health and they are presently emerging or accelerating, in most developing countries. One major lifestyle consequence is light at night and subsequent disrupted circadian rhythms commonly referred to as circadian disruption or chronodisruption. Mounting evidence reveals that particularly melatonin rhythmicity has crucial roles in a variety of metabolic functions as an anti-oxidant, anti-inflammatory chronobiotic and possibly as an epigenetic regulator. This paper provides a brief outline about metabolic dysregulation in conjunction with a disrupted melatonin rhythm.
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PMID:Role of melatonin in metabolic regulation. 1991 Dec 81

Vitamin D cannot be considered any more as only necessary to prevent rickets or osteomalacia. Calcitriol produced in the kidney is known to have classical endocrine phosphocalcic properties. More recently, vitamin D has been shown to play an important role in reducing the risk of many chronic diseases including type 2 diabetes mellitus, cardiovascular diseases, cancers, and autoimmune and infectious diseases. These effects may be secondary to local production of calcitriol and to its autocrine and paracrine actions on cellular proliferation and differentiation, apoptosis, insulin and renin secretion, interleukin and bactericidal proteins production. These pleiotropic effects are mostly documented by observational and experimental studies or small intervention trials that most often evaluated intermediate parameters. In renal transplant recipients, vitamin D insufficiency, defined as less than 30 ng/ml, is a frequent finding with more than 80% of patients displaying this profile. One may speculate that it could be a part of the explanation for the increased incidence of some complications observed after transplantation. Large intervention trials may therefore be of interest in this specific population.
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PMID:Potential nonclassical effects of vitamin D in transplant recipients. 2009 73

Vitamin D cannot any more be considered as exclusively necessary to prevent rickets or osteomalacia. Calcitriol produced in the kidney is known to have classical endocrine phosphocalcic properties. However, many other tissues express both vitamin D receptor and 1a-hydroxylase and can convert 25-hydroxy vitamin D into calcitriol. Calcitriol produced locally is considered to have autocrine and paracrine actions on cellular proliferation and differentiation, apoptosis, insulin and renin secretion, interleukin and bactericidal proteins production. Epidemiologic and experimental data argue in favour of a protective role of vitamin D against cancers, type 2 diabetes, cardiovascular, auto-immune and infectious diseases, chronic kidney disease and loss of muscular strength. A few interventional studies confirm the protective effect of vitamin D against cancers, intermediate markers of cardiovascular risk, epidemic influenza, albuminuria and risk of fall. We present here the non phosphocalcic actions of vitamin D.
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PMID:[Non phosphocalcic actions of vitamin D]. 2041 48

The prevalence of chronic non-communicable disease, such as type 2 diabetes mellitus (T2DM), is rising worldwide. In Africa, T2DM is primarily affecting those living in urban areas and increasingly affecting the poor. Diabetes management among urban poor is an area of research that has received little attention. Based on ethnographic fieldwork in Dar es Salam, the causes and conditions for diabetes management in Tanzania have been examined. In this paper, we focus on the structural context of diabetes services in Tanzania; the current status of biomedical and ethnomedical health care; and health-seeking among people with T2DM. We demonstrate that although Tanzania is actively developing its diabetes services, many people with diabetes and low socioeconomic status are unable to engage continuously in treatment. There are many challenges to be addressed to support people accessing diabetes health care services and improve diabetes management.
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PMID:"For someone who's rich, it's not a problem". Insights from Tanzania on diabetes health-seeking and medical pluralism among Dar es Salaam's urban poor. 2044 75

Infection with hepatitis C virus (HCV) primarily causes chronic liver disease with characteristic histopathologic features, including hepatic steatosis. Moreover, chronic hepatitis C is also closely related to insulin resistance (IR) and an increased risk of type 2 diabetes mellitus (DM). This review summarizes the available clinical evidence for a linkage of chronic HCV infection and developing IR or DM that comprises (i) retro- and prospective clinical studies, (ii) the excess risk of chronic hepatitis C patients to develop DM compared to hepatitis B patients, (iii) a preferential relationship of IR with HCV type-1, -2 or -4 infections, (iv) a correlation between IR, viral load and responsiveness to antiviral treatment and (v) a decreased incidence of DM in chronic hepatitis C after sustained virological response. This review further refers to the clinical evidence of a preferential relationship between hepatic steatosis and HCV type-3 infection, and that two distinct genotype-specific pathogenic mechanisms underlie steatosis in hepatitis C. In HCV type-3 infections, steatosis is related to viral load but not to metabolic factors, and, thus, is termed 'viral steatosis'. In HCV type-1, -2 or -4 infections, steatosis appears to be secondary to IR and regarded as 'metabolic steatosis'. In conclusion, multiple lines of clinical evidence support a linkage of HCV infection and both hepatic carbohydrate and lipid metabolism. The extent to which targeting the host's metabolism by drugs or by lifestyle change translates into an improvement of health or in a better response to interferon-alpha will provide further valuable insights into virus-host interactions, and is topic which is currently addressed in clinical studies.
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PMID:Hepatitis C virus, diabetes and steatosis: clinical evidence in favor of a linkage and role of genotypes. 2046 Sep 24

Failure of the functional pancreatic beta-cell mass to expand in response to increased metabolic demand is a hallmark of type 2 diabetes. Lineage tracing studies indicate that replication of existing beta-cells is important for beta-cell proliferation in adult animals. In rat pancreatic beta-cell lines (RIN5F), treatment with 100 nM thyroid hormone (triiodothyronine, T(3)) enhances cell proliferation. This result suggests that T(3) is required for beta-cell proliferation or replication. To identify the role of thyroid hormone receptor alpha (TR(alpha)) in the processes of beta-cell growth and cell cycle regulation, we constructed a recombinant adenovirus vector, AdTR(alpha). Infection with AdTR(alpha) to RIN5F cells increased the expression of cyclin D1 mRNA and protein. Overexpression of the cyclin D1 protein in AdTR(alpha)-infected cells led to activation of the cyclin D1/cyclin-dependent kinase/retinoblastoma protein/E2F pathway, along with cell cycle progression and cell proliferation following treatment with 100 nM T(3). Conversely, lowering cellular cyclin D1 by small interfering RNA knockdown in AdTR(alpha)-infected cells led to down-regulation of the cyclin D1/CDK/Rb/E2F pathway and inhibited cell proliferation. Furthermore, in immunodeficient mice with streptozotocin-induced diabetes, intrapancreatic injection of AdTR(alpha) led to the restoration of islet function and to an increase in the beta-cell mass. These results support the hypothesis that liganded TR(alpha) plays a critical role in beta-cell replication and in expansion of the beta-cell mass during postnatal development. Thus, liganded TR(alpha) may be a target for therapeutic strategies that can induce the expansion and regeneration of beta-cells.
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PMID:Liganded thyroid hormone receptor-alpha enhances proliferation of pancreatic beta-cells. 2052 52

The majority of all deliveries worldwide take place in the so-called developing world. Most recent epidemiological data have shown that the number of cases of type 2 diabetes mellitus and diabetes in pregnancy is steadily increasing worldwide. However, little is known about the prevalence of gestational diabetes in East Africa. Intrauterine exposure to the metabolic environment of maternal diabetes increases the risk of altered glucose homeostasis in the offspring, producing a higher prevalence of gestational diabetes mellitus in the next generation. Our preliminary results from an East African tertiary referral center show that in the year 2007 3.1% of all newborns had a birth weight of more than 4,000 g (mean 4,300 g, range 4,000- 5,600 g). During the same time period, the mean birth weight in the general population was only 3,046 g (range 600-3,200 g). Hence, personal experience in East Africa has convinced the authors that diabetes in pregnancy is grossly neglected. Besides infectious diseases like HIV/AIDS, the African continent is increasingly facing metabolic diseases such as type 2 diabetes mellitus and diabetes in pregnancy.
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PMID:[Gestational diabetes in East Africa: a mostly disregarded disease?]. 2053 Sep 39

Nowadays Russia faces problems, which are specific for the majority of the developed countries with respect to demography and health status. They are: low birth rate, ageing of the population and increase in prevalence of chronic non-infectious diseases (arterial hypertension, heart attacks, cerebral strokes, type 2 diabetes, oncological diseases etc.). But unlike these countries, Russia has retained rather a high mortality rate and a small length of life. The article analyses factors, which influenced this process. The conclusions prove the fact that an "unhealthy" lifestyle plays the primer role in deteriorating the population health in the Russian Federation, including incompliance of healthy nutrition principles.
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PMID:[Population health in the Russian Federation: risk factors and role of healthy nutrition]. 2056 Apr 82

The objective of the present review is to provide an overview of the metabolic effects of pro-inflammatory cytokine production during infection and injury; to highlight the disadvantages of pro-inflammatory cytokine production and inflammatory stress on morbidity and mortality of patients; to identify the influence of genetics and adiposity on inflammatory stress in patients and to indicate how nutrients may modulate the inflammatory response in patients. Recent research has shown clearly that adipose tissue actively secretes a wide range of pro- and anti-inflammatory cytokines. Paradoxically, although inflammation is an essential part of the response of the body to infection, surgery and trauma, it can adversely affect patient outcome. The metabolic effects of inflammation are mediated by pro-inflammatory cytokines. Metabolic effects include insulin insensitivity, hyperlipidaemia, muscle protein loss and oxidant stress. These effects, as well as being present during infective disease, are also present in diseases with a covert inflammatory basis. These latter diseases include obesity and type 2 diabetes mellitus. Inflammatory stress also increases during aging. The level of cytokine production, within individuals, is influenced by single nucleotide polymorphisms (SNP) in cytokine genes. The combination of SNP controls the relative level of inflammatory stress in both overt and covert inflammatory diseases. The impact of cytokine genotype on the intensity of inflammatory stress derived from an obese state is unknown. While studies remain to be done in the latter context, evidence shows that these genomic characteristics influence morbidity and mortality in infectious disease and diseases with an underlying inflammatory basis and thereby influence the cost of in-patient obesity. Antioxidants and n-3 PUFA alter the intensity of the inflammatory process. Recent studies show that genotypic factors influence the effectiveness of immunonutrients. A better understanding of this aspect of nutrient-gene interactions and of the genomic factors that influence the intensity of inflammation during disease will help in the more effective targeting of nutritional therapy.
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PMID:The true cost of in-patient obesity: impact of obesity on inflammatory stress and morbidity. 2059 96


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