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Stephan Rössner

Researcher at Karolinska Institutet

Publications -  105
Citations -  4315

Stephan Rössner is an academic researcher from Karolinska Institutet. The author has contributed to research in topics: Weight loss & Cholesterol. The author has an hindex of 32, co-authored 105 publications receiving 4173 citations. Previous affiliations of Stephan Rössner include Cancer Epidemiology Unit.

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Association of Weight Gain in Infancy and Early Childhood with Metabolic Risk in Young Adults

TL;DR: Rapid weight gain during infancy but not during early childhood (3-6 yr) predicted clustered metabolic risk at age 17 yr, and early interventions to moderate rapid weight gain even at very young ages may help to reduce adult cardiovascular disease risks.
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Does excess pregnancy weight gain constitute a major risk for increasing long-term BMI?

TL;DR: The objective was to assess the relevance of the recommendations of the Institute of Medicine, regarding gestational weight gain (GWG) for long-term BMI development for long‐ term BMI development.
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Glucagon-like peptide 1 increases the period of postprandial satiety and slows gastric emptying in obese men.

TL;DR: GLP-1 given exogenously at the start of a meal did not seem to affect meal termination or the amount of food eaten, however, postprandial feelings of hunger decreased, suggesting that exogenous GLP- 1 may influencefeelings of hunger and satiety in humans.
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Effects of a high-protein meal (meat) and a high-carbohydrate meal (vegetarian) on satiety measured by automated computerized monitoring of subsequent food intake, motivation to eat and food preferences.

TL;DR: The food-preference lists showed that before lunch there was relative preference for high-protein foods in favour of high-carbohydrate foods, but after lunch either meal produced instead a relative 'aversion' for high -protein foods, which was greater after theHigh-protein lunch meal than after the high- carbohydrate lunch meal.
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Catecholamine resistance in fat cells of women with upper-body obesity due to decreased expression of beta 2-adrenoceptors.

TL;DR: Lipolytic catecholamine resistance is present in abdominal obesity, due to low density of beta2-adrenoceptors, which in its turn may be caused by a post-transcriptional defect inbeta2-receptor expression.