Apparent epidemic of insulin-dependent diabetes mellitus in Midwestern Poland

Rewers, M.; Re, LaPorte; Walczak, Mieczysław; Dmochowski, K.; Bogaczynska, E.

doi:10.2337/diabetes.36.1.106

Cited by 61 publications

(25 citation statements)

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“…First, and perhaps most important, is the observation that the concordance rates for T1D in monozygotic twins is ~50% [74][75][76]. Second, epidemiological studies demonstrate that there is a significant increase in the incidence of T1D over the past 50 years in many countries, an increase that cannot be explained solely on the basis of genetic alterations [77][78][79]. Reports of epidemic outbreaks of T1D further implicate environmental factors in the etiology of T1D [79][80][81].…”

Section: Viruses and T1dmentioning

confidence: 95%

“…Second, epidemiological studies demonstrate that there is a significant increase in the incidence of T1D over the past 50 years in many countries, an increase that cannot be explained solely on the basis of genetic alterations [77][78][79]. Reports of epidemic outbreaks of T1D further implicate environmental factors in the etiology of T1D [79][80][81]. Third, migration studies show that the incidence of diabetes in offspring of individuals who had moved from a low-incidence to a high-incidence country is increased compared with the incidence recorded in the country of origin [82,83].…”

Section: Viruses and T1dmentioning

confidence: 99%

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The Role of Toll-Like Receptor Pathways in the Mechanism of Type 1 Diabetes

Lien¹,

Zipris²

2009

CMM

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Toll-like receptors (TLRs) and the innate immune system play a key role in sensing and eliminating microbial infections. Interactions between TLRs and their ligands expressed by microbial pathogens induce a cascade of intracellular signaling events, culminating in the upregulation of proinflammatory pathways. Over the past two decades, numerous studies have established the role of the acquired immune system in the mechanism triggering type 1 diabetes (T1D). The recent discovery of TLRs has led to the recognition that the innate immune system may act, under some circumstances, as a double-edged sword. In addition to its beneficial role in host defense, it may lead to upregulation of proinflammatory autoimmune responses, islet destruction and diabetes. Indeed, recent observations are consistent with the hypothesis that altered innate functions exist in patients with T1D and could be part of the mechanism leading to disease onset, but the underlying mechanisms and the relevance of these alterations to early events triggering disease remain to be identified. Data obtained from mouse and rat models of T1D implicated TLR pathways in both disease induction and prevention. In both the NOD mouse and diabetes-prone BB (BBDP) rat, TLR upregulation can suppress disease. In the BioBreeding Diabetes Resistant (BBDR) rat, however, diabetes induced by virus infection involves the upregulation of TLR9 pathways, and generic TLR upregulation synergizes with virus infection on diabetes induction. Studies performed in mouse models of T1D with spontaneous or induced T1D implicate TLR1, TLR2, TLR3, and TLR7 in disease mechanisms. The finding that TLR pathways are involved in mediating islet inflammation holds great promise for identifying new molecules that could potentially be targeted to specifically suppress the autoimmune process in individuals at high risk for disease development. The potential link between TLR upregulation and autoimmunity emphasizes the need for caution in using new therapies involving TLR agonists as vaccine adjuvants.

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Section: Viruses and T1dmentioning

confidence: 95%

Section: Viruses and T1dmentioning

confidence: 99%

The Role of Toll-Like Receptor Pathways in the Mechanism of Type 1 Diabetes

Lien¹,

Zipris²

2009

CMM

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“…Most [8,[22][23][24][25][26], but not all [27][28][29][30][31], population-based registries showed an increasing incidence of T1D over time. An updated report from the DIAMOND project examined the trends in incidence of T1D from 1990 to 1999 in 114 populations from 57 countries.…”

Section: Trends In the Incidence Of T1dmentioning

confidence: 99%

The Value of National Diabetes Registries: SEARCH for Diabetes in Youth Study

2010

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Diabetes mellitus is one of the most common severe chronic diseases of childhood. Much of our knowledge of the epidemiology of diabetes in young people has been generated by large collaborative efforts based on standardized registry data, such as the DIAMOND Project worldwide and the EURODIAB study in Europe. These registries showed that although at the start of the 20th century childhood diabetes was rare, by the end of the century a steady increase in incidence had been reported in many parts of the world. However, epidemiologic data for temporal trends in pediatric diabetes are still lacking or are minimal for most of the global population of youth, including in the United States. In addition, the epidemiology of diabetes in youth is changing. As youth are becoming increasingly overweight, we are seeing more obese children with a clinical phenotype of type 2 diabetes or "adult-onset" diabetes. It is imperative that efforts directed at surveillance of diabetes in young people continue and expand, not only to understand its complex etiology, but also because of its increasing public health importance.

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“…For example, there is a close to six-fold gradient in the incidence of type 1 diabetes between Russian Karelia and neighboring Finland, although the predisposing HLA-DQ genotypes are equally frequent in the two populations [17]. Third, there are many reports of local or regional "epidemics" of T1D in geographic pattern best explained by environmental exposure [18][19][20][21][22][23]. Taken together, these findings are consistent with a model of genetic susceptibility influenced by non-genetic factors of roughly equal magnitude.…”

Section: Introductionmentioning

confidence: 97%

Environmental factors in the development of Type 1 diabetes

Peng

Hagopian

2007

Rev Endocr Metab Disord

113

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Environmental factors appear to play an important role in the pathogenesis of childhood-onset type 1 diabetes (T1D). The most important factors are thought to be infectious, dietary, perinatal, and psychosocial. Enteroviruses (especially Coxsackie B virus), breastfeeding, the early presence or lack of certain foods, birth weight, childhood over-nutrition, maternal islet autoimmunity, and negative stress events have been shown to be related to the prevalence of T1D. However, clear conclusions to date are limited because most studies lacked power to detect exposure/disease associations, were not prospective or long-term, did not start in infancy, had imprecise or infrequent exposure estimates, had confounding exposures, and failed to account for genetic susceptibility. In addition to the identification of specific antigenic triggers, several more general hypotheses, including the accelerator and hygiene hypotheses, are testable approaches worth pursuing.

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Apparent epidemic of insulin-dependent diabetes mellitus in Midwestern Poland

Cited by 61 publications

References 0 publications

The Role of Toll-Like Receptor Pathways in the Mechanism of Type 1 Diabetes

The Role of Toll-Like Receptor Pathways in the Mechanism of Type 1 Diabetes

The Value of National Diabetes Registries: SEARCH for Diabetes in Youth Study

Environmental factors in the development of Type 1 diabetes

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