Time trends in the incidence of type 1 diabetes in Finnish children: a cohort study.
ABSTRACT Finland has the highest incidence of type 1 diabetes worldwide, reaching 40 per 100,000 people per year in the 1990s. Our aim was to assess the temporal trend in type 1 diabetes incidence since 2000 in Finnish children aged younger than 15 years and to predict the number of cases of type 1 diabetes in the future.
Children with newly diagnosed type 1 diabetes in Finland who were listed on the National Public Health Institute diabetes register, Central Drug Register, and Hospital Discharge Register in 1980-2005 were included in a cohort study. We excluded patients with type 2 diabetes and diabetes occurring secondary to other conditions, such as steroid use, Down's syndrome, and congenital malformations of pancreas.
10,737 children-5816 boys and 4921 girls-were diagnosed with type 1 diabetes before 15 years of age during 1980-2005. The average age-standardised incidence was 42.9 per 100,000 per year (95% CI 42.6-44.3) during this period, increasing from 31.4 per 100,000 per year in 1980 to 64.2 per 100,000 per year in 2005. The age-specific rates per 100,000 per year were 31.0, 50.5, and 50.6 at ages 0-4 years, 5-9 years, and 10-14-years, respectively. We noted a significant non-linear component to the time trend (p<0.0003). In children aged 0-4 years, the increase was largest, at 4.7% more affected every year. The overall boy-to-girl ratio of incidence was 1.1; at the age of 13 years, it was 1.7 (1.4-2.0). The predicted cumulative number of new cases with type 1 diabetes before 15 years of age between 2006 and 2020 was about 10 800.
The incidence of type 1 diabetes in Finnish children is increasing even faster than before. The number of new cases diagnosed at or before 14 years of age will double in the next 15 years and the age of onset will be younger (0-4 years).
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ABSTRACT: ndividuals with Diabetes Mellitus (DM) present marked reduction in sperm quality and higher DNA damage in spermatozoa, evidencing that this metabolic disorder impairs male fertility. These effects are related to defective testicular metabolic pathways and signaling, resulting in altered sperm metabolism. Spermatozoa metabolize several substrates to ensure energy supplies and any alteration in this feature compromises sperm quality. For ATP production, spermatozoa require substrate availability and the involvement of specific hexoses membrane carriers. DM is known to modulate the spermatozoa substrate consumption and/or production due to altered glycolytic behavior. In fact, glucose uptake and metabolism is highly deregulated in diabetic individuals. Herein, we present an overview of the implications of DM in sperm glucose uptake and metabolism. The understanding of these processes is essential to identify key mechanisms associated with DM-related male (in)fertility. Moreover, it may contribute to the development of therapeutics to counteract the dysfunction induced by DM in sperm metabolism.Molecular and Cellular Endocrinology 08/2014; DOI:10.1016/j.mce.2014.08.005 · 4.24 Impact Factor
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ABSTRACT: Diabetes mellitus (DM) is described as a metabolic disorder characterized by hyperglycaemia resulting from defective insulin secretion, resistance to insulin, or both, and represents one of the greatest threats to modern global health as its incidence is rapidly rising worldwide. Type 1 DM results from an absolute deficiency of insulin due to an autoimmune destruction of the pancreatic beta cells while type 2 DM is characterized by impaired insulin secretion and increased insulin resistance. It is well known that glucose regulation is crucial for normal spermatogenesis and fertility. In this process, insulin plays a crucial role since its dysfunction is connected with decreased cellular glucose transport. Both clinical and experimental reports suggest that fertility is highly decreased in patients or animals with DM. Both DM types impair male fertility and numerous studies in male diabetic individuals have demonstrated a marked reduction in fecundity, as well as impairment of sperm quality and higher percentage of spermatozoa with nuclear DNA damage. All these effects are known to be related with metabolic signaling pathways in testis that results in defective sperm metabolism. The different regions and structures of the sperm flagellum are of great importance because the metabolic pathways are compartmentalized in them. Spermatozoa metabolize several substrates as energy sources, such as hexoses (glucose, mannose, and fructose) or other metabolites (lactate and citrate). Any alteration in the ability of the spermatozoa to utilize substrates involved in ATP production is expected to compromise motility and subsequently fertility. For glycolysis to occur in sperm, these cells need specific carriers to transport energy sources through the cellular membrane, namely glucose transporters (GLUTs). DM is known to modulate spermatozoa substrate consumption and/or production due to altered glycolysis. The transport of hexoses via GLUTs is also known to be highly dysregulated in diabetic male individuals. Throughout this chapter we will discuss the effects of DM in sperm glucose uptake and metabolism. Understanding the functioning and regulation of these processes is crucial to identify the key mechanisms associated with male (in)fertility in order to develop possible therapeutics.Glucose Uptake: Regulation, Signaling Pathways and Health Implications, Endocrinology Research and Clinical Developments edited by Carter C. Johnson, Davis B. Williams, 10/2013: chapter Implications of Diabetes on Sperm Glucose Uptake and Metabolism; Nova Publishers., ISBN: 978-1-62618-671-2
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ABSTRACT: Type 1 diabetes (T1D) is an autoimmune disease mediated by T cells that selectively destroy the insulin-producing β cells. Previous reports based on epidemiological and animal studies have demonstrated that both genetic factors and environmental parameters can either promote or attenuate the progression of autoimmunity. In recent decades, several inbred rodent strains that spontaneously develop diabetes have been applied to the investigation of the pathogenesis of T1D. Because the genetic manipulation of mice is well developed (transgenic, knockout, and conditional knockout/transgenic), most studies are performed using the nonobese diabetic (NOD) mouse model. This paper will focus on the use of genetically manipulated NOD mice to explore the pathogenesis of T1D and to develop potential therapeutic approaches.Journal of Diabetes Research 03/2013; 2013:138412. DOI:10.1155/2013/138412 · 3.54 Impact Factor