Speciality
Spotlight

       




 


Medicine


   

 




Obesity

   

  • Minerva

    BMJ,
    v
    ol.7254,
    15th July 2000


       

    Scientists
    from Johns Hopkins University in Baltimore have
    developed a new molecule that regulates appetite.
    The fatty acid synthetase inhibitor C75 regulates
    appetite so well that mice treated with it drop
    their food intake by 90% [Science 2000;288:2379-81].
    They also lose a lot of weight. The new molecule may
    or may not be the answer to rampaging human obesity;
    researchers are already gearing up to find out.

      

  • Thorkild IA Sorensen

    Obesity genes

    BMJ, Vol.322, 17 March 2001, p.630-631



    Obesity is influenced by environmental factors and by genetics. That obesity runs in families is an old observation. The pattern of inheritance suggests that the effect is polygenic, with each variant of many different genes making a small difference in effect. As a phenotype obesity is also heterogeneous and there are 2 distinct but frequently overlapping subtypes: general obesity and abdominal obesity. These subtypes have different physiological, clinical and prognostic implications. The phenotypes seem to have some of the same genetic and environmental influences in common.



    Since the identification of the leptin gene, many other single genes have also been investigated as candidates for causing obesity, and the entire genome has been scanned for loci associated with obesity. A few genes have been found to cause monogenic forms of obesity in humans.



    One way forward may be to conduct controlled human experiments by manipulating environmental factors that are assumed to be pertinent, such as fat intake. Its effect on both gene expression and the function of gene products in people with different genetic variants may elucidate which genes contribute to common obesity.

      

  • Roland Rosmond, Claude Bouchard, et al 

    Tsp5091 polymorphism in exon 2 of the glucocorticoid receptor gene in relation to obesity and cortisol secretion: cohort study.

    BMJ, Vol.322, 17 March 2001, p.652-653



    Chronically elevated cortisol levels can increase body fat, as seen in Cushing’s syndrome. Subjects with abdominal obesity share many of the hormonal, metabolic and circulatory characteristics of people with Cushing’s syndrome. A dysfunctional glucocorticoid receptor may add to the adverse health effects of excessive cortisol concentrations.



    An Asn363Ser polymorphism in exon 2 of the glucocorticoid receptor gene (GRL) might be associated with overweight and an increased sensitivity to exogenous glucocorticoids. Authors examined whether this variant was associated with altered sensitivity to glucocorticoids as well as obesity with its related metabolic and haemodynamic abnormalities in a cohort of Swedish men.



    It was concluded that GRL has several different polymorphisms and mutations, but that few of these are consistently associated with obesity and subtle physiological alterations in the hypothalamic-pituitary adrenal axis regulating cortisol secretion. The Asn363Ser polymorphism does not seem to be one of the variants associated with such changes.





        

 



 

           

Speciality Spotlight

       

 
Medicine
   

 

Obesity
   

  • Minerva
    BMJ, vol.7254, 15th July 2000
       
    Scientists from Johns Hopkins University in Baltimore have developed a new molecule that regulates appetite. The fatty acid synthetase inhibitor C75 regulates appetite so well that mice treated with it drop their food intake by 90% [Science 2000;288:2379-81]. They also lose a lot of weight. The new molecule may or may not be the answer to rampaging human obesity; researchers are already gearing up to find out.
      

  • Thorkild IA Sorensen
    Obesity genes
    BMJ, Vol.322, 17 March 2001, p.630-631

    Obesity is influenced by environmental factors and by genetics. That obesity runs in families is an old observation. The pattern of inheritance suggests that the effect is polygenic, with each variant of many different genes making a small difference in effect. As a phenotype obesity is also heterogeneous and there are 2 distinct but frequently overlapping subtypes: general obesity and abdominal obesity. These subtypes have different physiological, clinical and prognostic implications. The phenotypes seem to have some of the same genetic and environmental influences in common.

    Since the identification of the leptin gene, many other single genes have also been investigated as candidates for causing obesity, and the entire genome has been scanned for loci associated with obesity. A few genes have been found to cause monogenic forms of obesity in humans.

    One way forward may be to conduct controlled human experiments by manipulating environmental factors that are assumed to be pertinent, such as fat intake. Its effect on both gene expression and the function of gene products in people with different genetic variants may elucidate which genes contribute to common obesity.
      

  • Roland Rosmond, Claude Bouchard, et al 
    Tsp5091 polymorphism in exon 2 of the glucocorticoid receptor gene in relation to obesity and cortisol secretion: cohort study.
    BMJ, Vol.322, 17 March 2001, p.652-653

    Chronically elevated cortisol levels can increase body fat, as seen in Cushing’s syndrome. Subjects with abdominal obesity share many of the hormonal, metabolic and circulatory characteristics of people with Cushing’s syndrome. A dysfunctional glucocorticoid receptor may add to the adverse health effects of excessive cortisol concentrations.

    An Asn363Ser polymorphism in exon 2 of the glucocorticoid receptor gene (GRL) might be associated with overweight and an increased sensitivity to exogenous glucocorticoids. Authors examined whether this variant was associated with altered sensitivity to glucocorticoids as well as obesity with its related metabolic and haemodynamic abnormalities in a cohort of Swedish men.

    It was concluded that GRL has several different polymorphisms and mutations, but that few of these are consistently associated with obesity and subtle physiological alterations in the hypothalamic-pituitary adrenal axis regulating cortisol secretion. The Asn363Ser polymorphism does not seem to be one of the variants associated with such changes.


        

 

 

By |2022-07-20T16:41:59+00:00July 20, 2022|Uncategorized|Comments Off on Obesity

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