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Blockade of the glu...
Blockade of the glucocorticoid receptor with RU 486: effects in vitro and in vivo on human adipose tissue lipoprotein lipase activity.
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- Ottosson, Malin, 1959 (författare)
- Gothenburg University,Göteborgs universitet,Wallenberglaboratoriet,Wallenberg Laboratory
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- Mårin, Per (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin,Institute of Internal Medicine
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- Karason, Kristjan, 1962 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för kroppssammansättning och metabolism,Institute of Internal Medicine, Dept of Body Composition and Metabolism
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visa fler...
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- Elander, Anna, 1955 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för de kirurgiska disciplinerna, Avdelningen för plastikkirurgi,Institute of Surgical Sciences, Department of Plastic Surgery
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- Björntorp, Per, 1931 (författare)
- Gothenburg University,Göteborgs universitet,Wallenberglaboratoriet,Wallenberg Laboratory
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visa färre...
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(creator_code:org_t)
- 1995
- 1995
- Engelska.
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Ingår i: Obesity research. - 1071-7323. ; 3:3, s. 233-40
- Relaterad länk:
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https://gup.ub.gu.se...
Abstract
Ämnesord
Stäng
- Cortisol is known to induce lipoprotein lipase (LPL) activity in human adipose tissue in vitro and in vivo such as in Cushing's syndrome. The significance of the glucocorticoid receptor (GR) for this induction was evaluated in the present study. The synthetic steroid molecule RU 486, a potent glucocorticoid antagonist, was used as a tool to block the GR, in vitro and in vivo. In addition to LPL activity, glucose tolerance, blood pressure and plasma lipids, all variables influenced by cortisol, were studied in order to evaluate the peripheral antiglucocorticoid activity of RU 486 in vivo, in man. Addition of both cortisol and RU 486 to incubations of human adipose tissue pieces significantly inhibited the increase in LPL activity that could be induced by cortisol alone (p < 0.01). In a ten-fold molarity excess RU 486 totally abolished cortisol action (p < 0.01). With cortisol and RU 486 in equimolar concentrations the RU 486 blockade was probably incomplete and LPL activity induced (p < 0.05). The results imply that the stimulating effect of cortisol on LPL activity in human adipose tissue is mediated via the GR. Administration of 400 mg RU 486 at 2200 hours on two consecutive days to healthy men caused a significant rise in serum cortisol levels measured at 0800 hours (p < 0.05). The mean LPL activity in the subcutaneous abdominal adipose tissue remained unchanged. The mean level of serum triglycerides decreased significantly (p < 0.01) and there was a negative correlation between change in LPL activity and change in triglyceride levels (r = -0.73, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Endokrinologi och diabetes (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Endocrinology and Diabetes (hsv//eng)
Nyckelord
- Adipose Tissue
- metabolism
- Adolescent
- Adult
- Blood Glucose
- analysis
- Blood Pressure
- drug effects
- Body Mass Index
- Female
- Humans
- Hydrocortisone
- blood
- In Vitro Techniques
- Insulin
- metabolism
- Lipids
- blood
- Lipoprotein Lipase
- metabolism
- Male
- Middle Aged
- Mifepristone
- pharmacology
- Receptors
- Glucocorticoid
- antagonists & inhibitors
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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