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Oluf Borbye Pedersen

Publications and source records attributed to Oluf Borbye Pedersen.

7 recordsLinked to original sources
PubMed2006

[The genetics of obesity].

Although environmental factors clearly play a role, studies of twins and adoptees show that obesity is a familial trait which to a large degree can be ascribed to genetic factors. According to evolutionary models, obesity-causing variants may originally have had an evolutionary benefit, whereas in a modern environment they pose a risk. Despite a clear genetic cause, the molecular genetic variations underlying common forms of obesity are not clear. Out of many hundred candidates, only a few hold up, and only variations in the MC4R gene have been found with a prevalence which may lead to common forms of obesity.

Genetic Predisposition to Disease↗
PubMed2006

[Molecular pathogenesis in monogenic and polygenic obesity].

During the last few years, studies of the molecular pathogenesis of obesity both in mouse models and in the rare cases of monogenic obesity in humans have added significantly to our understanding of the key role of the hypothalamus in mediating hunger and satiety. These insights have brought us closer to the development of rational therapies of obesity, the epidemic of which is continuing in the post-industrial society, which is characterised by sedentary behaviour patterns.

Animals↗
PubMed2005

A statistical approach based on substitution of macronutrients provides additional information to models analyzing single dietary factors in relation to type 2 diabetes in danish adults: the Inter99 study.

Most studies analyzing diet-disease relations focus on single dietary factors rather than combining different nutrients into the same statistical model. The objective of this study was to identify dietary factors associated with the probability of having diabetes identified by screening (SDM) in Danish men and women aged 30-60 y. A specific objective was to examine whether an alternative statistical approach could provide additional information to already existing statistical approaches used in nutritional epidemiology. Baseline data from the Danish population-based Inter99 study were used. The dietary intake of 262 individuals with SDM was compared with that of 4627 individuals with normal glucose tolerance (NGT) using 2 different types of multiple logistic regression models adjusted for potential confounders. The first model included single dietary factors, whereas the second model was based on substitution of macronutrients. In the models with single dietary factors, high intakes of carbohydrates, dietary fiber, and coffee were inversely associated with SDM (P < 0.01), whereas high intakes of total fat and saturated fat were positively associated with SDM (P < 0.05). A modest U-shaped association was found between alcohol consumption and SDM (P = 0.10) [corrected] Results from the substitution model showed that when 3% of energy (En%) as carbohydrate replaced 3 En% fat or alcohol, the probability of having SDM decreased by 9 and 10%, respectively (P < 0.01) [corrected] No other macronutrient substitutions resulted in significant associations. Hence, the statistical approach based on substitution of macronutrients provided additional information to the model analyzing single dietary factors.

Adult↗
PubMed2002

[Maturity-onset diabetes of the young--MODY. Molecular-genetic, pathophysiological and clinical characteristics].

Maturity-onset diabetes of the young (MODY) is a genetically and clinically heterogeneous subtype of type 2 diabetes characterised by an early onset, an autosomal dominant inheritance, and a primary defect in insulin secretion. MODY comprises 2-5% of cases of type 2 diabetes. So far, six MODY genes have been identified (MODY1-6): hepatocyte nuclear factor (HNF-4 alpha), glucokinase, HNF-1 alpha, HNF-1 beta, insulin promoter factor 1(IPF-1), and neurogenic differentiation factor 1 (NEUROD1). MODY2 and MODY3 are the most common forms of MODY. Mutations in glucokinase/MODY2 result in a mild form of diabetes. In contrast, MODY3 and some of the other MODY forms are characterised by major insulin secretory defects and severe hyperglycaemia associated with microvascular complications. About 25% of known MODY is caused by mutations in yet unknown genes and present results suggest that other monogenic forms of type 2 diabetes might exist. The diagnosis of MODY has implications for the clinical management of the patient's diabetes. The identification of MODY genes also opens new perspectives in the understanding of the molecular basis of diabetes and may probably contribute to the definition of novel targets for drug development and gene therapy.

Diabetes Mellitus, Type 2↗