Global Prevalence of Diabetes: Estimates for the Year 2000 and Projections for 2030

Rathmann, Wolfgang; Giani, Guido

doi:10.2337/diacare.27.10.2568

Cited by 370 publications

(231 citation statements)

References 4 publications

Supporting

Mentioning

203

Contrasting

Unclassified

Order By: Relevance

“…The World Health Organization (WHO) estimates that there will be more than 550 million cases by 2030. These patients are predisposed to cardiovascular morbidity and mortality (Rathmann & Giani, 2004). Cardiovascular events account for two‐thirds of the mortality in patients with diabetes (Boudina & Abel, 2007).…”

Section: Introductionmentioning

confidence: 99%

Glucagon‐like peptide‐1 ameliorates cardiac lipotoxicity in diabetic cardiomyopathy via the PPARα pathway

Wang

et al. 2018

Aging Cell

View full text Add to dashboard Cite

SummaryLipotoxicity cardiomyopathy is the result of excessive accumulation and oxidation of toxic lipids in the heart. It is a major threat to patients with diabetes. Glucagon‐like peptide‐1 (GLP‐1) has aroused considerable interest as a novel therapeutic target for diabetes mellitus because it stimulates insulin secretion. Here, we investigated the effects and mechanisms of the GLP‐1 analog exendin‐4 and the dipeptidyl peptidase‐4 inhibitor saxagliptin on cardiac lipid metabolism in diabetic mice (DM). The increased myocardial lipid accumulation, oxidative stress, apoptosis, and cardiac remodeling and dysfunction induced in DM by low streptozotocin doses and high‐fat diets were significantly reversed by exendin‐4 and saxagliptin treatments for 8 weeks. We found that exendin‐4 inhibited abnormal activation of the (PPARα)‐CD36 pathway by stimulating protein kinase A (PKA) but suppressing the Rho‐associated protein kinase (ROCK) pathway in DM hearts, palmitic acid (PA)‐treated rat h9c2 cardiomyocytes (CMs), and isolated adult mouse CMs. Cardioprotection in DM mediated by exendin‐4 was abolished by combination therapy with the PPARα agonist wy‐14643 but mimicked by PPARα gene deficiency. Therefore, the PPARα pathway accounted for the effects of exendin‐4. This conclusion was confirmed in cardiac‐restricted overexpression of PPARα mediated by adeno‐associated virus serotype‐9 containing a cardiac troponin T promoter. Our results provide the first direct evidence that GLP‐1 protects cardiac function by inhibiting the ROCK/PPARα pathway, thereby ameliorating lipotoxicity in diabetic cardiomyopathy.

show abstract

Section: Introductionmentioning

confidence: 99%

Glucagon‐like peptide‐1 ameliorates cardiac lipotoxicity in diabetic cardiomyopathy via the PPARα pathway

Wang

et al. 2018

Aging Cell

View full text Add to dashboard Cite

show abstract

“…No sensitivity analysis was performed for the WHO estimates of diabetes prevalence used for these calculations (6), and we have not speculated on the possible range. However, subsequent studies have shown that the WHO study probably underestimated the prevalence of diabetes (23), and, consequently, these mortality estimates are likely to be conservative.…”

Section: Validationmentioning

confidence: 99%

The Burden of Mortality Attributable to Diabetes

et al. 2005

View full text Add to dashboard Cite

OBJECTIVE -To estimate the global number of excess deaths due to diabetes in the year 2000.RESEARCH DESIGN AND METHODS -We used a computerized generic formal disease model (DisMod II), used by the World Health Organization to assess disease burden through modeling the relationships between incidence, prevalence, and disease-specific mortality. Baseline input data included population structure, age-and sex-specific estimates of diabetes prevalence, and available published estimates of relative risk of death for people with diabetes compared with people without diabetes. The results were validated with population-based observations and independent estimates of relative risk of death.RESULTS -The excess global mortality attributable to diabetes in the year 2000 was estimated to be 2.9 million deaths, equivalent to 5.2% of all deaths. Excess mortality attributable to diabetes accounted for 2-3% of deaths in poorest countries and over 8% in the U.S., Canada, and the Middle East. In people 35-64 years old, 6 -27% of deaths were attributable to diabetes.CONCLUSIONS -These are the first global estimates of mortality attributable to diabetes. Globally, diabetes is likely to be the fifth leading cause of death. Diabetes Care 28:2130 -2135, 2005D iabetes is a serious illness with multiple complications and premature mortality, accounting for at least 10% of total health care expenditure in many countries (1). However, routinely reported statistics based on death certification seriously underestimate mortality from diabetes (2), because individuals with diabetes most often die of cardiovascular and renal disease and not from a cause uniquely related to diabetes, such as ketoacidosis or hypoglycemia (3).Most international mortality statistics, including those published by the World Health Organization (WHO), are based solely on the "underlying cause of death" as recorded on the death certificate, even in the presence of other information. Complex methods have been developed for estimating cause-specific mortality for some conditions (AIDS, tuberculosis) but not for diabetes (4).Based on routine statistics, recent World Health Reports estimated mortality from diabetes in the world as 987,000 deaths for the year 2002 (5), which was 1.7% of total world mortality. There were estimated to be at least 170 million people with diabetes in the world in the year 2000 (6); therefore, mortality attributable to diabetes could be expected to be much higher, since diabetes is a serious and chronic condition. The aim of this study was to provide a more realistic estimate of the number of deaths attributable to diabetes. RESEARCH DESIGN AND METHODS Model and dataTo estimate the number of deaths attributable to diabetes in the year 2000, we used a software program, DisMod II, developed for the Global Burden of Disease 2000 study (7,8) and routinely used by WHO for disease estimates. The DisMod II disease model is that of a multistate life table that describes a single disease. There are two causes of death, from the disease and from "all othe...

show abstract

“…The number of patients with diabetes mellitus (DM), a metabolic disorder, is rapidly increasing worldwide due to several factors: population growth, aging, urbanization, increasing prevalence of obesity and reduced physical activity [ 1 ] . Increased oxidative stress (OS) may have an important causal role in β-cell failure and the development of insulin resistance, it is believed to be related with the onset and progression of diabetes.…”

mentioning

confidence: 99%

Blood ALDH1 and GST Activity in Diabetes Type 2 and its Correlation with Glycated Hemoglobin

Giebułtowicz

Sołobodowska

Bobilewicz

et al. 2014

Exp Clin Endocrinol Diabetes

View full text Add to dashboard Cite

tive stress-associated pathologies. Excessive levels of LDAs are decreased by several enzyme systems that are able to oxidize them to acids like aldehyde dehydrogenase (ALDH) or catalyze their conjugation with endogenous ligands like glutathione-S-transferase (GST) [ 5 ] . There are only a few studies on erythrocyte glutathione S-transferase (GST) activity in DM, the results of which are ambiguous. Jerntorp et al. tried to fi nd an association between ALDH activity and DM and its complications such as large vessel disease, but the method they used did not lead to any valid conclusions [ 6 , 7 ] . Therefore, the aim of our studies was to compare the ALDH1 and GST activity in whole blood of DM patients and healthy control and analyze the relation of those enzymes activity with HbA1c. Materials and Methods ▼ Patients64 DM type 2 patients of the Warsaw Medical University Hospital (Group 1) and 60 healthy controls from the out-patients clinic (Control group) were enrolled in this study. Introduction ▼The number of patients with diabetes mellitus (DM), a metabolic disorder, is rapidly increasing worldwide due to several factors: population growth, aging, urbanization, increasing prevalence of obesity and reduced physical activity [ 1 ] . Increased oxidative stress (OS) may have an important causal role in β-cell failure and the development of insulin resistance, it is believed to be related with the onset and progression of diabetes. Moreover, OS also results from hyperglycemia associated with diabetes. Therefore, it is considered as a factor related to diabetes complications [ 2 ] . It is highly probable that not only reactive oxygen species (ROS) themselves but also secondary by-products of lipid peroxidation (LP) contribute to the deleterious consequences of OS e. g. insulin resistance [ 3 ] . Lipid peroxidationderived aldehydes (LDAs) may also increase the incidence of DM complications by the modifi cation of the collagen of the cardiovascular system causing its stiff ening and changes in the charge profi le [ 4 ] . This emphasizes the importance of the cellular protective mechanisms against LADs as they can prevent the development of some oxida-

show abstract

Global Prevalence of Diabetes: Estimates for the Year 2000 and Projections for 2030

Cited by 370 publications

References 4 publications

Glucagon‐like peptide‐1 ameliorates cardiac lipotoxicity in diabetic cardiomyopathy via the PPARα pathway

Glucagon‐like peptide‐1 ameliorates cardiac lipotoxicity in diabetic cardiomyopathy via the PPARα pathway

The Burden of Mortality Attributable to Diabetes

Blood ALDH1 and GST Activity in Diabetes Type 2 and its Correlation with Glycated Hemoglobin

Contact Info

Product

Resources

About