Is leptin the parabiotic "satiety" factor? Past and present interpretations

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

In 1959 Hervey hypothesized that a circulating feedback signal informed the hypothalamus of the size of fat stores and initiated appropriate corrections to energy balance. The hypothesis resulted from a parabiosis study in which one animal became obese following lesioning of the ventromedial hypothalamus. The partner of the lesioned rat was hypophagic and lost a large amount of body fat. Similar results came from parabiosis studies with obese Zucker rats and rats that overate due to stimulation of the lateral hypothalamus. In studies in which one parabiont was made obese by overfeeding the non-overfed partners lost substantial amounts of fat with a minimal reduction in food intake and no loss of lean tissue. The loss of fat was due to inhibition of adipose lipogenesis and other metabolic adjustments typical of food restriction. Parabiosis with genetically obese mice implied that ob/ob mice did not produce the feedback signal and subsequently the mutant ob protein, leptin, was identified. This paper provides a review and interpretation of parabiosis work that preceded the discovery of leptin, an evaluation of leptin in relation to its function as the circulating feedback signal and evidence for additional circulating factors involved in the control of adipose tissue mass.

Original languageEnglish (US)
Pages (from-to)111-118
Number of pages8
JournalAppetite
Volume61
DOIs
StatePublished - Feb 1 2013

Fingerprint

Parabiosis
Leptin
Fats
Hypothalamus
Adipose Tissue
Lateral Hypothalamic Area
Zucker Rats
Obese Mice
Lipogenesis
Mutant Proteins
Eating
Food

Keywords

  • Body composition
  • Hypothalamus
  • Leptin
  • Obesity
  • Parabiosis

ASJC Scopus subject areas

  • Psychology(all)
  • Nutrition and Dietetics

Cite this

Is leptin the parabiotic "satiety" factor? Past and present interpretations. / Harris, Ruth Babette.

In: Appetite, Vol. 61, 01.02.2013, p. 111-118.

Research output: Contribution to journalArticle

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