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Björn Forsén

Publications -  10
Citations -  6158

Björn Forsén is an academic researcher. The author has contributed to research in topics: Type 2 diabetes & Diabetes mellitus. The author has an hindex of 8, co-authored 10 publications receiving 5939 citations.

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Cardiovascular Morbidity and Mortality Associated With the Metabolic Syndrome

TL;DR: The WHO definition of the metabolic syndrome identifies subjects with increased cardiovascular morbidity and mortality and offers a tool for comparison of results from diferent studies.
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Clinical and genetic characteristics of type 2 diabetes with and without GAD antibodies.

TL;DR: GADab+ patients differ from both GADab- type 2 diabetic patients and type 1 diabetic patients with respect to beta-cell function, features of the metabolic syndrome, and type1 diabetes susceptibility genes, and it is proposed that LADA be defined as GADAB positivity (>5 relative units) in patients older than 35 years at onset of type 2 diabetes.
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Metabolic Consequences of a Family History of NIDDM (The Botnia Study): Evidence for Sex-Specific Parental Effects

TL;DR: It is concluded that abdominal obesity, insulin resistance, and decreased resting metabolic rate are characteristic features of first-degree relatives of patients with NIDDM and that the decrease in resting metabolic rates is partially related to the degree of abdominal obesity.
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Predictors of and Longitudinal Changes in Insulin Sensitivity and Secretion Preceding Onset of Type 2 Diabetes

TL;DR: A marked deterioration in beta-cell function precedes the onset of type 2 diabetes and these individuals can be identified early by knowledge of FPG, BMI, and family history of diabetes.
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A family history of diabetes is associated with reduced physical fitness in the Prevalence, Prediction and Prevention of Diabetes (PPP)–Botnia study

TL;DR: Individuals with a family history of type 2 diabetes are characterised by lower physical fitness, which cannot solely be explained byLower physical activity, and have an impaired capacity of beta cells to compensate for an increase in insulin resistance imposed by an increases in BMI.