Level of satiety

In vitro energy metabolism in brain during hypophagic and hyperphagic body weight recovery

T. R. Kasser, Ruth Babette Harris, R. J. Martin

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Rates of in vitro glucose and fatty acid oxidation were examined in four brain sites during hypophagic and hyperphagic recovery of normal body weight. Rats were fed 40, 100, or 160% of normal intake, via gastric intubation, for 3 wk. Another group of rats were starved until body weight loss was equivalent to weight loss in 40%-fed rats. Groups of rats were killed at the conclusion of tube feeding or fasting and at specific periods during recovery of body weight. Brain sites examined were the ventrolateral hypothalamus (VLH), ventromedial hypothalamus (VMH), a caudal brain stem site encompassing the area postrema-nucleus of the solitary tract (AP-NTS), and cortex. During recovery, rats previously fed 160% of normal intake (anorectic) maintained low rates of VLH fatty acid oxidation and were hypophagic until most excess fat was depleted. Conversely, rats previously fed 40% of normal intake (hungry) maintained high rates of VLH fatty acid oxidation and were hyperphagic until most deficient fat was repleted. Rats previously starved maintained high rates of VLH fatty acid oxidation during hyperphagic recovery, although levels of VLH fatty acid oxidation and food intake were initially low on refeeding. Rates of glucose oxidation in the brain sites examined did not relate well to energy balance status and the needed adjustments in food intake. The results indicated that the level of glucose oxidation in the VLH and AP-NTS responded to the level of energy immediately coming into the system (food intake). These data support the concept that the level of VLH fatty acid oxidation is inversely proportional to the level of peripheral fat storage and that high or low rates of VLH fatty acid may be a component of the mechanism that elicits the compensatory hyperphagic or hypophagic response, respectively.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume257
Issue number6
StatePublished - Dec 1 1989
Externally publishedYes

Fingerprint

Energy Metabolism
Hypothalamus
Body Weight
Fatty Acids
Brain
Area Postrema
Solitary Nucleus
Eating
Fats
Glucose
Weight Loss
Social Adjustment
In Vitro Techniques
Ideal Body Weight
Appetite Depressants
Enteral Nutrition
Intubation
Brain Stem
Fasting
Stomach

Keywords

  • body weight regulation
  • brain metabolism
  • food intake control

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

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title = "Level of satiety: In vitro energy metabolism in brain during hypophagic and hyperphagic body weight recovery",
abstract = "Rates of in vitro glucose and fatty acid oxidation were examined in four brain sites during hypophagic and hyperphagic recovery of normal body weight. Rats were fed 40, 100, or 160{\%} of normal intake, via gastric intubation, for 3 wk. Another group of rats were starved until body weight loss was equivalent to weight loss in 40{\%}-fed rats. Groups of rats were killed at the conclusion of tube feeding or fasting and at specific periods during recovery of body weight. Brain sites examined were the ventrolateral hypothalamus (VLH), ventromedial hypothalamus (VMH), a caudal brain stem site encompassing the area postrema-nucleus of the solitary tract (AP-NTS), and cortex. During recovery, rats previously fed 160{\%} of normal intake (anorectic) maintained low rates of VLH fatty acid oxidation and were hypophagic until most excess fat was depleted. Conversely, rats previously fed 40{\%} of normal intake (hungry) maintained high rates of VLH fatty acid oxidation and were hyperphagic until most deficient fat was repleted. Rats previously starved maintained high rates of VLH fatty acid oxidation during hyperphagic recovery, although levels of VLH fatty acid oxidation and food intake were initially low on refeeding. Rates of glucose oxidation in the brain sites examined did not relate well to energy balance status and the needed adjustments in food intake. The results indicated that the level of glucose oxidation in the VLH and AP-NTS responded to the level of energy immediately coming into the system (food intake). These data support the concept that the level of VLH fatty acid oxidation is inversely proportional to the level of peripheral fat storage and that high or low rates of VLH fatty acid may be a component of the mechanism that elicits the compensatory hyperphagic or hypophagic response, respectively.",
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T2 - In vitro energy metabolism in brain during hypophagic and hyperphagic body weight recovery

AU - Kasser, T. R.

AU - Harris, Ruth Babette

AU - Martin, R. J.

PY - 1989/12/1

Y1 - 1989/12/1

N2 - Rates of in vitro glucose and fatty acid oxidation were examined in four brain sites during hypophagic and hyperphagic recovery of normal body weight. Rats were fed 40, 100, or 160% of normal intake, via gastric intubation, for 3 wk. Another group of rats were starved until body weight loss was equivalent to weight loss in 40%-fed rats. Groups of rats were killed at the conclusion of tube feeding or fasting and at specific periods during recovery of body weight. Brain sites examined were the ventrolateral hypothalamus (VLH), ventromedial hypothalamus (VMH), a caudal brain stem site encompassing the area postrema-nucleus of the solitary tract (AP-NTS), and cortex. During recovery, rats previously fed 160% of normal intake (anorectic) maintained low rates of VLH fatty acid oxidation and were hypophagic until most excess fat was depleted. Conversely, rats previously fed 40% of normal intake (hungry) maintained high rates of VLH fatty acid oxidation and were hyperphagic until most deficient fat was repleted. Rats previously starved maintained high rates of VLH fatty acid oxidation during hyperphagic recovery, although levels of VLH fatty acid oxidation and food intake were initially low on refeeding. Rates of glucose oxidation in the brain sites examined did not relate well to energy balance status and the needed adjustments in food intake. The results indicated that the level of glucose oxidation in the VLH and AP-NTS responded to the level of energy immediately coming into the system (food intake). These data support the concept that the level of VLH fatty acid oxidation is inversely proportional to the level of peripheral fat storage and that high or low rates of VLH fatty acid may be a component of the mechanism that elicits the compensatory hyperphagic or hypophagic response, respectively.

AB - Rates of in vitro glucose and fatty acid oxidation were examined in four brain sites during hypophagic and hyperphagic recovery of normal body weight. Rats were fed 40, 100, or 160% of normal intake, via gastric intubation, for 3 wk. Another group of rats were starved until body weight loss was equivalent to weight loss in 40%-fed rats. Groups of rats were killed at the conclusion of tube feeding or fasting and at specific periods during recovery of body weight. Brain sites examined were the ventrolateral hypothalamus (VLH), ventromedial hypothalamus (VMH), a caudal brain stem site encompassing the area postrema-nucleus of the solitary tract (AP-NTS), and cortex. During recovery, rats previously fed 160% of normal intake (anorectic) maintained low rates of VLH fatty acid oxidation and were hypophagic until most excess fat was depleted. Conversely, rats previously fed 40% of normal intake (hungry) maintained high rates of VLH fatty acid oxidation and were hyperphagic until most deficient fat was repleted. Rats previously starved maintained high rates of VLH fatty acid oxidation during hyperphagic recovery, although levels of VLH fatty acid oxidation and food intake were initially low on refeeding. Rates of glucose oxidation in the brain sites examined did not relate well to energy balance status and the needed adjustments in food intake. The results indicated that the level of glucose oxidation in the VLH and AP-NTS responded to the level of energy immediately coming into the system (food intake). These data support the concept that the level of VLH fatty acid oxidation is inversely proportional to the level of peripheral fat storage and that high or low rates of VLH fatty acid may be a component of the mechanism that elicits the compensatory hyperphagic or hypophagic response, respectively.

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