Regulation of Energy Balance

Hervey, G. R.

doi:10.1038/222629a0

Cited by 177 publications

(65 citation statements)

References 18 publications

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“…The marked overexpression of the ob gene in C57Bl/6J ob/ob adipose tissue further suggested that the gene was under feedback control, with an increased level of gene expression in the obese state, consistent with the data from the classic parabiosis experiments by Coleman (15). However, Coleman's experiments did not predict where the hormone that was missing in ob mice was expressed, though prior experiments from Hervey predicted that the receptor would be expressed in the hypothalamus (20).…”

Section: Wiring Diagram Of a Complex Behaviorsupporting

confidence: 70%

The long road to leptin

Friedman¹

2016

Journal of Clinical Investigation

228

190

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Section: Wiring Diagram Of a Complex Behaviorsupporting

confidence: 70%

The long road to leptin

Friedman¹

2016

Journal of Clinical Investigation

228

190

View full text Add to dashboard Cite

“…Implicit in this hypothesis was the prediction that the ob gene was under feedback control and that obesity would be associated with increased levels of ob RNA. However, Coleman's experiments did not predict where the hormone that was missing in ob mice was expressed, though prior experiments from Hervey predicted that the receptor would be expressed in the hypothalamus (Hervey 1969).…”

Section: Introductionmentioning

confidence: 95%

20 YEARS OF LEPTIN: Leptin at 20: an overview

Friedman¹

2014

Journal of Endocrinology

204

146

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Historically, adipose tissue was considered to be a passive storage vessel discharging nutrients in times of famine and accumulating fat in times of surfeit. This view changed with the identification of leptin as an adipocyte hormone. Leptin functions as an afferent signal in a negative feedback loop that regulates food intake and metabolism to maintain homeostatic control of adipose tissue mass. Before this, the existence of a system maintaining homeostatic control of energy balance was unclear. The identification of leptin has thus uncovered a new endocrine system that also links changes in nutrition to adaptive responses in most if not all other physiologic systems. Further studies have revealed a set of clinical syndromes caused by leptin deficiency, including lipodystrophy and hypothalamic amenorrhea. This work has led to new therapeutic approaches for a number of human conditions and has also established a conceptual framework for studying the pathogenesis of obesity.

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“…Kennedy, 1953 argued for feedback information reaching the hypothalamus from adipose tissue, which he argued is closely monitored through the sensitivity of the hypothalamus to the concentration of circulating metabolites. Hervey in 1969 proposed a mechanism for lipostatic regulation, based on endogenous measurement of the fat mass by means of a fat soluble hormone that monitors adipose tissue mass by the dilution principle (Hervey, 1969). Experiments in the late 1970s using genetically obese rodents and parabiotic regimes (Coleman 1978) created the conceptual context for the studies that have led to the identi®cation of the protein`Leptin' (Zhang et al, 1994), which is currently the subject of remarkable scienti®c scrutiny.…”

Section: Appetite Control Mechanisms Which Limit Cho and Fat Intakesmentioning

confidence: 99%

High and low carbohydrate and fat intakes: limits imposed by appetite and palatability and their implications for energy balance

Blundell

Stubbs²

1999

Eur J Clin Nutr

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This report examines several issues concerning the effects of dietary fats and carbohydrates (CHOs) on body weight and the limits set on the intake of these nutrients by factors in¯uencing appetite control: (i) the physiological relationship between feeding behaviour (FB) and body weight; (ii) the distribution of nutrients in Western foods and the implications this may have for FB; (iii) the contribution of nutrients in the diet, to total EI under both extreme and typical Western conditions; (iv) the known effects that fats, CHOs and dietary energy density (ED) exert on appetite and energy balance (EB); (v) the potential role of sensory factors in promoting or limiting fat, CHO and energy intakes (EI) in modern human populations Population studies and large surveys have identi®ed individuals with wide ranges of fat and CHO intakes. Intakes of fat can vary from an average of 180 gaday to 25 gaday in a representative sample. But on individual days fat intake can rise to well over 200 g according to a selection of high fat foods. In a single meal, people can consume an amount of fat greater than the population daily average. From this analysis it can be deduced that the appetite control mechanism will permit the consumption of large amounts of fat (if an abundance of high fat foods exist in the food supply). Except for speci®c physiological circumstances (e.g. endurance explorers) where there is an urgent need for EIs, in the face of decreasing body weight, it is unlikely that the body will generate a speci®c drive for fat. Because CHO foods have a lower ED than fat foods (on average) and because of their greater satiating capacity, the free intake of high CHO foods is likely to be self-limiting (at lower EIs than those generated by fatty foods). This does not mean that excess EIs are impossible when people feed ad libitum on high CHO diets.

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Regulation of Energy Balance

Cited by 177 publications

References 18 publications

The long road to leptin

The long road to leptin

20 YEARS OF LEPTIN: Leptin at 20: an overview

High and low carbohydrate and fat intakes: limits imposed by appetite and palatability and their implications for energy balance

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