Altered food intake in age-related anorexia: Evidence suggesting hypothalamic dysregulation

C. A. Blanton, Barbara A Horwitz, R. B. McDonald

Research output: Contribution to journalArticle

Abstract

Near the end of life in humans there occurs decreased food intake and a loss of body weight, both of which are associated with morbidity and mortality. We have established a model for investigating this "anorexia of aging" in rats where the onset of spontaneous rapid weight loss near the end of life serves as a biomarker for senescence. We have shown that age-related rapid weight loss is associated with decreased food intake, severe attenuation of cold-induced thermoregulation, and altered circadian rhythm of body temperature. These functions are, in part, under hypothalamic regulation. To further evaluate age-related anorexia, we measured feeding patterns in presenescent and senescent rats. Nine male F344 rats were monitored continuously from 25 months of age, when their body weight was stable, until 5-7 days after the onset of weight loss. Food intake (grams/day) was greater during weight stability (13.2 ± 0.29 g/day) than during weight loss (10.9 ± 0.33 g/day). This reflected smaller meal size (wt. stable, 1.35 ± 0.04 g/meal; wt. loss, 1.04 ± 0.03 g/meal) and shorter meal duration (wt. stable, 15.8 ± 0.74 min; wt. loss, 11.9 ± 0.59 min) without a change in number of meals/day. These findings suggest that senescent rats became satiated sooner than presenescent rats. As would be expected following reduced food intake and body fat loss, the senescent rats had lower concentrations of serum leptin (3.1 ± 0.39 ng/ml) and thyroxine (0.33 ± 0.04 ng/dl) than did the presenescent animals (6.0 ± 1.04 ng/ml; 0.60 ± 0.19 ng/dl, respectively). Yet the senescent rats were not hyperphagic, indicating a "disconnect" in the leptin-food intake regulatory pathway. Mechanisms underlying the anorexia of aging in rats appear to involve disruption of the hypothalamic regulation of food intake with respect to both satiation and "drive".

Original languageEnglish (US)
JournalFASEB Journal
Volume12
Issue number5
StatePublished - Mar 20 1998
Externally publishedYes

Fingerprint

Anorexia
anorexia
Rats
food intake
Eating
Meals
rats
Weight Loss
weight loss
hypothalamic regulation
Leptin
leptin
Body Weight
Satiation
Aging of materials
Appetite Regulation
Body Temperature Regulation
portion size
Inbred F344 Rats
Feeding Behavior

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

Altered food intake in age-related anorexia : Evidence suggesting hypothalamic dysregulation. / Blanton, C. A.; Horwitz, Barbara A; McDonald, R. B.

In: FASEB Journal, Vol. 12, No. 5, 20.03.1998.

Research output: Contribution to journalArticle

Blanton, C. A. ; Horwitz, Barbara A ; McDonald, R. B. / Altered food intake in age-related anorexia : Evidence suggesting hypothalamic dysregulation. In: FASEB Journal. 1998 ; Vol. 12, No. 5.
@article{8ee17b0c81e2476ebb94a0d53418d646,
title = "Altered food intake in age-related anorexia: Evidence suggesting hypothalamic dysregulation",
abstract = "Near the end of life in humans there occurs decreased food intake and a loss of body weight, both of which are associated with morbidity and mortality. We have established a model for investigating this {"}anorexia of aging{"} in rats where the onset of spontaneous rapid weight loss near the end of life serves as a biomarker for senescence. We have shown that age-related rapid weight loss is associated with decreased food intake, severe attenuation of cold-induced thermoregulation, and altered circadian rhythm of body temperature. These functions are, in part, under hypothalamic regulation. To further evaluate age-related anorexia, we measured feeding patterns in presenescent and senescent rats. Nine male F344 rats were monitored continuously from 25 months of age, when their body weight was stable, until 5-7 days after the onset of weight loss. Food intake (grams/day) was greater during weight stability (13.2 ± 0.29 g/day) than during weight loss (10.9 ± 0.33 g/day). This reflected smaller meal size (wt. stable, 1.35 ± 0.04 g/meal; wt. loss, 1.04 ± 0.03 g/meal) and shorter meal duration (wt. stable, 15.8 ± 0.74 min; wt. loss, 11.9 ± 0.59 min) without a change in number of meals/day. These findings suggest that senescent rats became satiated sooner than presenescent rats. As would be expected following reduced food intake and body fat loss, the senescent rats had lower concentrations of serum leptin (3.1 ± 0.39 ng/ml) and thyroxine (0.33 ± 0.04 ng/dl) than did the presenescent animals (6.0 ± 1.04 ng/ml; 0.60 ± 0.19 ng/dl, respectively). Yet the senescent rats were not hyperphagic, indicating a {"}disconnect{"} in the leptin-food intake regulatory pathway. Mechanisms underlying the anorexia of aging in rats appear to involve disruption of the hypothalamic regulation of food intake with respect to both satiation and {"}drive{"}.",
author = "Blanton, {C. A.} and Horwitz, {Barbara A} and McDonald, {R. B.}",
year = "1998",
month = "3",
day = "20",
language = "English (US)",
volume = "12",
journal = "FASEB Journal",
issn = "0892-6638",
publisher = "FASEB",
number = "5",

}

TY - JOUR

T1 - Altered food intake in age-related anorexia

T2 - Evidence suggesting hypothalamic dysregulation

AU - Blanton, C. A.

AU - Horwitz, Barbara A

AU - McDonald, R. B.

PY - 1998/3/20

Y1 - 1998/3/20

N2 - Near the end of life in humans there occurs decreased food intake and a loss of body weight, both of which are associated with morbidity and mortality. We have established a model for investigating this "anorexia of aging" in rats where the onset of spontaneous rapid weight loss near the end of life serves as a biomarker for senescence. We have shown that age-related rapid weight loss is associated with decreased food intake, severe attenuation of cold-induced thermoregulation, and altered circadian rhythm of body temperature. These functions are, in part, under hypothalamic regulation. To further evaluate age-related anorexia, we measured feeding patterns in presenescent and senescent rats. Nine male F344 rats were monitored continuously from 25 months of age, when their body weight was stable, until 5-7 days after the onset of weight loss. Food intake (grams/day) was greater during weight stability (13.2 ± 0.29 g/day) than during weight loss (10.9 ± 0.33 g/day). This reflected smaller meal size (wt. stable, 1.35 ± 0.04 g/meal; wt. loss, 1.04 ± 0.03 g/meal) and shorter meal duration (wt. stable, 15.8 ± 0.74 min; wt. loss, 11.9 ± 0.59 min) without a change in number of meals/day. These findings suggest that senescent rats became satiated sooner than presenescent rats. As would be expected following reduced food intake and body fat loss, the senescent rats had lower concentrations of serum leptin (3.1 ± 0.39 ng/ml) and thyroxine (0.33 ± 0.04 ng/dl) than did the presenescent animals (6.0 ± 1.04 ng/ml; 0.60 ± 0.19 ng/dl, respectively). Yet the senescent rats were not hyperphagic, indicating a "disconnect" in the leptin-food intake regulatory pathway. Mechanisms underlying the anorexia of aging in rats appear to involve disruption of the hypothalamic regulation of food intake with respect to both satiation and "drive".

AB - Near the end of life in humans there occurs decreased food intake and a loss of body weight, both of which are associated with morbidity and mortality. We have established a model for investigating this "anorexia of aging" in rats where the onset of spontaneous rapid weight loss near the end of life serves as a biomarker for senescence. We have shown that age-related rapid weight loss is associated with decreased food intake, severe attenuation of cold-induced thermoregulation, and altered circadian rhythm of body temperature. These functions are, in part, under hypothalamic regulation. To further evaluate age-related anorexia, we measured feeding patterns in presenescent and senescent rats. Nine male F344 rats were monitored continuously from 25 months of age, when their body weight was stable, until 5-7 days after the onset of weight loss. Food intake (grams/day) was greater during weight stability (13.2 ± 0.29 g/day) than during weight loss (10.9 ± 0.33 g/day). This reflected smaller meal size (wt. stable, 1.35 ± 0.04 g/meal; wt. loss, 1.04 ± 0.03 g/meal) and shorter meal duration (wt. stable, 15.8 ± 0.74 min; wt. loss, 11.9 ± 0.59 min) without a change in number of meals/day. These findings suggest that senescent rats became satiated sooner than presenescent rats. As would be expected following reduced food intake and body fat loss, the senescent rats had lower concentrations of serum leptin (3.1 ± 0.39 ng/ml) and thyroxine (0.33 ± 0.04 ng/dl) than did the presenescent animals (6.0 ± 1.04 ng/ml; 0.60 ± 0.19 ng/dl, respectively). Yet the senescent rats were not hyperphagic, indicating a "disconnect" in the leptin-food intake regulatory pathway. Mechanisms underlying the anorexia of aging in rats appear to involve disruption of the hypothalamic regulation of food intake with respect to both satiation and "drive".

UR - http://www.scopus.com/inward/record.url?scp=33749288922&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33749288922&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:33749288922

VL - 12

JO - FASEB Journal

JF - FASEB Journal

SN - 0892-6638

IS - 5

ER -