Site of action of putative lipostatic factor: Food intake and peripheral pentose shunt activity

Ruth Babette Harris, R. J. Martin

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Obesity due to overfeeding in one parabiotic rat results in mild hypophagia and specific loss of fat from its partner. Studies were conducted to determine whether the changes in body composition were reversible and whether the nonsignificant reduction food intake was a primary response to a humoral lipstatic factor. Tube feeding partners of overfed rats 0.5 g more food per day than eaten voluntarily prevented loss of fat, although hepatic and adipose glucose-6-phosphate dehydrogenase activities were depressed. Glucose flux through the pentose phosphate pathway was inhibited in both adipose and hepatic tissue from thin partners of obese rats, although fatty acid synthesis was depressed only in adipose tissue. Response to insulin by adipocytes from ad libitum partners of obese rats appeared to be blunted, but insulin sensitivity was normal. When overfeeding stopped, both partners returned to control body composition, suggesting that changes observed in parabiotic partners of obese rats were physiological responses to a putative circulating lipostatic factor rather than a nonspecific consequence of parabiosis.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume259
Issue number1 28-1
StatePublished - Jan 1 1990
Externally publishedYes

Fingerprint

Pentose Phosphate Pathway
Eating
Body Composition
Adipose Tissue
Parabiosis
Fats
Glucosephosphate Dehydrogenase
Liver
Enteral Nutrition
Adipocytes
Insulin Resistance
Fatty Acids
Obesity
Insulin
Glucose
Food

Keywords

  • Fatty acid synthesis
  • Humoral factor
  • Parabiotic rats

ASJC Scopus subject areas

  • Physiology

Cite this

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