Weight loss normalizes the inhibitory effect of N6-(phenylisopropyl)adenosine on lipolysis in fat cells of massively obese human subjects
Autor: | Pertti Mustajoki, Stanely P. Hreniuk, Kathryn F. LaNoue, Susanna Ranta, Jorma J. Ohisalo, Johanna Kaartinen, Louis F. Martin |
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Rok vydání: | 1992 |
Předmět: |
medicine.medical_specialty
Adenosine Deaminase Lipolysis Gastric Bypass Adipose tissue 030209 endocrinology & metabolism Biology 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Adenosine deaminase Weight loss Adipocyte Internal medicine Weight Loss medicine Humans Postoperative Period Cells Cultured 030304 developmental biology 2. Zero hunger 0303 health sciences General Medicine medicine.disease Adenosine Obesity Obesity Morbid Endocrinology Adipose Tissue chemistry Phenylisopropyladenosine biology.protein medicine.symptom Body mass index medicine.drug |
Zdroj: | Clinical Science. 83:589-592 |
ISSN: | 1470-8736 0143-5221 |
DOI: | 10.1042/cs0830589 |
Popis: | 1. Fat cells were isolated from massively obese patients at or before gastric bypass, from other patients after normalization of body weight after gastric bypass or gastroplasty (post-bypass patients) and from control subjects of a stable normal body weight. 2. The inhibition of isoprenaline-stimulated lipolysis by N6-(phenylisopropyl)adenosine in the presence of adenosine deaminase was much attenuated in cells from the massively obese patients as compared with those from normal-weight control subjects, but was normal in cells from post-bypass patients. 3. Isolated fat cells of the massively obese patients were larger (913 ± 197 pl, mean ± sem) than those of the normal-weight group (437 ± 95 pl). The volume of cells from the post-bypass patients was only 125 ± 49 pl, although the body mass index of this group was almost exactly the same as that of the normal-weight control subjects. 4. Although epidemiological studies have suggested that genetic factors are important in the development and maintenance of obesity, these results demonstrate that the changes observed in the inhibitory regulation of lipolysis in obesity are secondary. |
Databáze: | OpenAIRE |
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