Physiological Regulation

Of the total energy expenditure for DIT, about one-third is ascribable to stimulation of BAT or to futile cycles to produce extra heat. Thus, DIT consists of adaptive thermogenesis together with thermogenesis induced by cold exposure. This adaptive thermogenesis, which responds to temperature and diet, is highly variable and is influenced by genetic makeup. It is regulated by brain activity throughout the sympathetic nervous system (SNS), an important efferent pathway.

p-Adrenergic receptors (pARS) transmit the thermogenetic signal to peripheral target tissue (brown fat, and possibly muscle and other tissues) and play an important role in diet-induced ther-mogenesis and therefore also in prevention of diet-induced obesity. Various components of the energy balance system in the brain have been identified and include the leptin receptor, melanocyte stimulating hormone (MSH), the melanocortin-4 receptor (MC4 receptor), neuropeptide Y (NPY), and agouti-related protein (AgRP) (Fig. 2) [6]. Alterations in DIT may be of great importance in controlling body weight and in promoting obesity, as indicated by the fact that most animal models of obesity (ob/ob, db/db and MC-4 receptor gene knock-out mice) have defects in adaptive thermogenesis.

The amount of DIT depends on the nutrient composition of the foods ingested and on the total amount of energy introduced. Higher energy requirements for subjects with higher physical activity or greater body dimensions correspond to higher energy expenditures in absolute values for digestion, absorption, and storage of ingested nutrients. Measurement of the energetic cost of DIT is not simple, since it is difficult to separate

Fig. 2. Pathway for diet-induced thermogenesis. The brain receives signals from diet and adipose tissue. Neuronal circuits controlling energy expenditure are activated, which, in turn, increase sympathetic nerve activity. Brown adipose tissue is one effector of sympathetically driven thermogenesis. Other tissues, such as skeletal muscle, are also likely to be important effectors. AgRP, agouti-related protein; MC4 receptor, melanocortin 4 receptor; MCH, melanin-concentrating hormone; MSH, a-melanocyte-stimulating hormone; NPY, neuropeptide Y

Fig. 2. Pathway for diet-induced thermogenesis. The brain receives signals from diet and adipose tissue. Neuronal circuits controlling energy expenditure are activated, which, in turn, increase sympathetic nerve activity. Brown adipose tissue is one effector of sympathetically driven thermogenesis. Other tissues, such as skeletal muscle, are also likely to be important effectors. AgRP, agouti-related protein; MC4 receptor, melanocortin 4 receptor; MCH, melanin-concentrating hormone; MSH, a-melanocyte-stimulating hormone; NPY, neuropeptide Y

the amount of energy expenditure above BM after a meal from the energetic cost due to physical activity related to sitting, eating, and digesting. In practical terms, DIT is determined by measuring the metabolism of subjects after a meal, without limiting small movements. The value so obtained represents the resting metabolic rate (RMR), which is higher than the BM since it includes the energy expenditure for digestion and metabolism and for the increase in muscle tone and small movements. From measurements made in the morning, afternoon, and evening, it is possible to obtain an average value of the RMR [7].

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Dieting Dilemma and Skinny Solutions

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