An investigation of the Satiety Mechanism: A Research Initiative
Part I
Researched and Composed by Gabriel “Venom” Wilson, BSc. (Hons), CSCS
Abstract
The regulation of satiety is a complex subject beyond the reader’s wildest imaginations. Multitudes of hormones such as leptin and insulin play intricate roles in its regulation. The lateral and ventromedial hypothalamic areas of the brain are but a few anatomical aspects which relay information of hunger and satiation to the body. This entry strives to take the most comprehensive analysis ever of the mechanisms which regulate satiety and how they can be manipulated for the benefit of the athlete under various scenarios.
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Introduction
Meals
Meals are the basic measurement for caloric consumption due to the fact that the amount of food you consume is determined by the size and frequency of your meals. Three basic phases which affect your meals are hunger, satiation, and satiety. These aspects will be broken down subsequently.
Dual Center Hypothesis
Hunger may be defined as the sensation which drives an individual to find and consume food [1]. In 1940, Hetherington and Ranson postulated that feeding involved activation of the lateral hypothalamus (LHA). They found two areas of the hypothalamus that monitor feeding and body fat [2]. Shortly thereafter, the dual center hypothesis was invented [3]. This states that the LHA is responsible for hunger and subsequent feeding, while the ventromedial hypothalamus (VMH) is responsible for satiety and satiation. To clarify, after the ingestion of a certain amount of food, a suppression of hunger occurs that will lead to the termination of feeding. This is referred to as satiation. The feeling of fullness between meals is referred to as satiety [1].
Recent experiments have brought support to this hypothesis. For instance, studies show electrical impulses on the lateral hypothalamic area of animals results in feeding, while an impulse on the ventromedial aspect promotes satiation and eventual termination of feeding [4, 5, 6]. Moreover, it has been shown that harming the VMH leads to insulin resistance and hyperinsulinemia in animals. Further, subjects with an injured VMH eat an immense amount of excess calories, resulting in obesity [7, 8].
While the roles of the lateral and ventromedial hypothalamic areas are well established, the dual center hypothesis is simplistic to say the least. You see, there are many more mechanisms which control feeding and satiation. For instance, nuclei throughout the inferior brain stem collaborate and deliver messages to endocrine organs and forebrain structures. The midbrain and thalamus further interpret this information in accordance to the sensory properties of food, and the forebrain nuclei communicate the positive aspects of feeding. These feeding centers are informed by multitudes of hormonal and neural outputs on the metabolic stasis of the body [1, 9].
A variety of other factors such as insulin, neuropeptide Y, leptin, catecholamines, and ghrelin must be taken into account. Today we are going to discuss these factors and how you, the athlete, can properly manipulate them to achieve your goals.
Feeding Regulation
A multitude of elements can influence your caloric intake, but these can be simplified into two categories: anorexigenic and orexigenic factors. The former promotes a lack or loss of appetite for food, while the latter results in a desire for food. Some topics discussed will be a combination of both. We begin with the protein hormone leptin.
Leptin
Leptin is a protein hormone secreted from adipose tissue [10]. Since its discovery, leptin has been considered a contributor to satiety [11]. Multitudes of studies confirm this hypothesis. For instance, leptin reduced food consumption and body weight when given to rats intraperitoneally (administered by entering the peritoneum, which is the membrane that lines the cavity of the abdomen), intravenously (through veins), or intracerebrally (in the cerebrum) [12, 13, 14, 15, 16]. Furthermore, Chapelot et al. demonstrated that plasma leptin concentrations increase during spontaneous intermeal intervals, and decline before the onset of a meal, showing leptin may contribute to meal patterns [40].
Body fat is a huge factor in leptin concentrations. The amount of leptin secreted into the blood stream is largely dictated by how much fat one has. For example, leptin was measured in seventy-one obese individuals and 108 normal weighted ones [17]. Leptin in the latter group was measured at 8 ng/ml. Results showed the largest discrepancy occurred when body fat reached over 25%—increasing anywhere from three-tenfold.
Carbohydrates are also a potent leptin regulator. Insulin given to rats increases leptin gene expression, and inhibits the reduction in leptin mRNA caused by calorie restriction and fasting (i.e. 36 hours) [19, 20]. Similar effects have also been reported in humans [21, 22]. Glucose metabolism has been shown to be an important factor in leptin utilization; this may be why insulin stimulates leptin secretion [42].
To add to the comment on calorie restriction, a decrease of 10% in body weight has been shown to decrease leptin by 53% in some cases [29]. Moreover, a decrease in leptin during starvation diets will promote energy conservation by decreasing thyroid hormone-induced thermogenesis (one way is by decreasing NPY, discussed later) and increasing glucocorticoids that mobilize energy stores [1]. Brent et al. tested the interactions between energy intake and fat loss on plasma leptin during prolonged, moderate and severe energy restriction [43]. Mean leptin decreased markedly by up to 66% (P < r =" 0.51,">
Source: abcbodybuilding.com
Part I
Researched and Composed by Gabriel “Venom” Wilson, BSc. (Hons), CSCS
Abstract
The regulation of satiety is a complex subject beyond the reader’s wildest imaginations. Multitudes of hormones such as leptin and insulin play intricate roles in its regulation. The lateral and ventromedial hypothalamic areas of the brain are but a few anatomical aspects which relay information of hunger and satiation to the body. This entry strives to take the most comprehensive analysis ever of the mechanisms which regulate satiety and how they can be manipulated for the benefit of the athlete under various scenarios.
--------------------------------------------------------------------------------
Introduction
Meals
Meals are the basic measurement for caloric consumption due to the fact that the amount of food you consume is determined by the size and frequency of your meals. Three basic phases which affect your meals are hunger, satiation, and satiety. These aspects will be broken down subsequently.
Dual Center Hypothesis
Hunger may be defined as the sensation which drives an individual to find and consume food [1]. In 1940, Hetherington and Ranson postulated that feeding involved activation of the lateral hypothalamus (LHA). They found two areas of the hypothalamus that monitor feeding and body fat [2]. Shortly thereafter, the dual center hypothesis was invented [3]. This states that the LHA is responsible for hunger and subsequent feeding, while the ventromedial hypothalamus (VMH) is responsible for satiety and satiation. To clarify, after the ingestion of a certain amount of food, a suppression of hunger occurs that will lead to the termination of feeding. This is referred to as satiation. The feeling of fullness between meals is referred to as satiety [1].
Recent experiments have brought support to this hypothesis. For instance, studies show electrical impulses on the lateral hypothalamic area of animals results in feeding, while an impulse on the ventromedial aspect promotes satiation and eventual termination of feeding [4, 5, 6]. Moreover, it has been shown that harming the VMH leads to insulin resistance and hyperinsulinemia in animals. Further, subjects with an injured VMH eat an immense amount of excess calories, resulting in obesity [7, 8].
While the roles of the lateral and ventromedial hypothalamic areas are well established, the dual center hypothesis is simplistic to say the least. You see, there are many more mechanisms which control feeding and satiation. For instance, nuclei throughout the inferior brain stem collaborate and deliver messages to endocrine organs and forebrain structures. The midbrain and thalamus further interpret this information in accordance to the sensory properties of food, and the forebrain nuclei communicate the positive aspects of feeding. These feeding centers are informed by multitudes of hormonal and neural outputs on the metabolic stasis of the body [1, 9].
A variety of other factors such as insulin, neuropeptide Y, leptin, catecholamines, and ghrelin must be taken into account. Today we are going to discuss these factors and how you, the athlete, can properly manipulate them to achieve your goals.
Feeding Regulation
A multitude of elements can influence your caloric intake, but these can be simplified into two categories: anorexigenic and orexigenic factors. The former promotes a lack or loss of appetite for food, while the latter results in a desire for food. Some topics discussed will be a combination of both. We begin with the protein hormone leptin.
Leptin
Leptin is a protein hormone secreted from adipose tissue [10]. Since its discovery, leptin has been considered a contributor to satiety [11]. Multitudes of studies confirm this hypothesis. For instance, leptin reduced food consumption and body weight when given to rats intraperitoneally (administered by entering the peritoneum, which is the membrane that lines the cavity of the abdomen), intravenously (through veins), or intracerebrally (in the cerebrum) [12, 13, 14, 15, 16]. Furthermore, Chapelot et al. demonstrated that plasma leptin concentrations increase during spontaneous intermeal intervals, and decline before the onset of a meal, showing leptin may contribute to meal patterns [40].
Body fat is a huge factor in leptin concentrations. The amount of leptin secreted into the blood stream is largely dictated by how much fat one has. For example, leptin was measured in seventy-one obese individuals and 108 normal weighted ones [17]. Leptin in the latter group was measured at 8 ng/ml. Results showed the largest discrepancy occurred when body fat reached over 25%—increasing anywhere from three-tenfold.
Carbohydrates are also a potent leptin regulator. Insulin given to rats increases leptin gene expression, and inhibits the reduction in leptin mRNA caused by calorie restriction and fasting (i.e. 36 hours) [19, 20]. Similar effects have also been reported in humans [21, 22]. Glucose metabolism has been shown to be an important factor in leptin utilization; this may be why insulin stimulates leptin secretion [42].
To add to the comment on calorie restriction, a decrease of 10% in body weight has been shown to decrease leptin by 53% in some cases [29]. Moreover, a decrease in leptin during starvation diets will promote energy conservation by decreasing thyroid hormone-induced thermogenesis (one way is by decreasing NPY, discussed later) and increasing glucocorticoids that mobilize energy stores [1]. Brent et al. tested the interactions between energy intake and fat loss on plasma leptin during prolonged, moderate and severe energy restriction [43]. Mean leptin decreased markedly by up to 66% (P < r =" 0.51,">
Source: abcbodybuilding.com