Body Weight Set-Points: Determination and Adjustment

Abstract

It is proposed that body weight, like body water and body temperature, is physiologically regulated. In the case of body weight, coordinated adjustments in both the intake and expenditure of energy serve to stabilize the weights of individuals at a specified level and to resist their displacement from this level. Obese individuals also display these behavioral and metabolic adjustments to weight perturbations and thus appear to actively resist efforts to reduce their weight from the elevated levels they ordinarily display. Experimental studies of genetically transmitted and diet-induced forms of obesity in animals similarly suggest a view of obesity as a condition of body energy regulation at an elevated set-point. An individual's set-point for regulated body weight is apparently adjustable, shifting over a lifespan in conjunction with naturally occurring but still unspecified physiologic changes. Experimentally, the set-point for body weight can be adjusted by manipulation of specific hypothalamic sites. Lesions of the lateral hypothalamus, for example, cause a chronic reduction in the level at which laboratory animals regulate body weight. It thus appears that hypothalamic mechanisms play a primary role in setting the level at which individuals regulate body weight, and it is likely that the genetic, dietary and other lifespan influences on body weight are expressed through these mechanisms.

Developmental programming of lipid metabolism and aortic vascular function in C57BL/6 mice: a novel study suggesting an involvement of LDL-receptor

“…Previous studies have reported increased adiposity and body weight in male and female offspring of mothers fed an SFA-rich diet during pregnancy and lactation in different rat models (9,27,37). It has also been shown earlier that rodents, like humans, can regulate their food intake and energy expenditure to maintain a set body weight (33). This would explain the reduction of food intake in the case of S/S and C/S offspring.…”

Leptin reduces food intake but does not alter weight regain following food deprivation in the rat

“…The 'set point' has been proposed as a body weight that is physiologically regulated, where intake and expenditure of energy are adjusted in order to maintain this level. 5,6 Supporting this are observations that deprived animals and humans usually re-gain their weight after dietary restraints are removed. 6,7 There are a number of central effector pathways in the hypothalamus involved in regulating appetite which are thought to be influenced by body adiposity, resulting in long-term stability of fat stores.…”

“…5,6 Supporting this are observations that deprived animals and humans usually re-gain their weight after dietary restraints are removed. 6,7 There are a number of central effector pathways in the hypothalamus involved in regulating appetite which are thought to be influenced by body adiposity, resulting in long-term stability of fat stores. 1 The concept that humoral signals generated in proportion to body fat stores, act in the brain to regulate body weight and adiposity 8 was strengthened by the discovery of mutations in obese mice 9,10 and, subsequently, the discovery of leptin.…”

Predictive Adaptive Responses to Maternal High-Fat Diet Prevent Endothelial Dysfunction but Not Hypertension in Adult Rat Offspring

“…However, food intake was less in male and female FF than in male and female FC and CON (Figure 4). Rats are known to regulate caloric intake when fed a hypercaloric diet, 18 and despite reduced dietary intake, fat intake remained 4-fold higher in FF rats compared with controls. When dietary intake in offspring was converted to energy, the average daily gross energy intake increased only in male FF (average daily intake after 60 days of age, 393.07Ϯ6.66 kJ, nϭ5 versus CON, 362.22Ϯ5.54 kJ, nϭ10; PϽ0.05), and this is a likely explanation for the increase in body weight by 180 days.…”