Obesity is a multifaceted problem with many contributing factors including but not limited to genetics, hormone levels, overconsumption of food, and sedentary lifestyle. The estimated prevalence of obesity in the USA is 72.5 million adults with costs attributed to obesity more than 147 billion dollars per year. Dietary adherence has been shown to be negatively associated with the degree of caloric restriction [1]. Though caloric restriction has been used extensively in weight control studies, short-term success has been difficult to achieve, with long-term success of weight control being even more elusive. In light of this evidence, development of strategies to promote weight loss in the absence of purposeful caloric restriction could be advantageous in the battle against obesity. Since obesity is viewed as a multi-faceted problem, this paper proposes several different lifestyle factors that may be modified in order to contribute to weight reduction in the absence of caloric restriction. These lifestyle factors are macronutrient composition of meals, meal frequency, exercise, sleep, and psychological stress. Therefore, novel approaches are needed to control the rates of obesity that are occurring globally. The purpose of this paper is to provide a synopsis of how exercise, sleep, psychological stress, and meal frequency and composition affect levels of ghrelin, cortisol, insulin GLP-1, and leptin and weight control. In particular, this paper focuses on how the manipulation of these lifestyle factors may positively or negatively influence ghrelin, glucocorticoids (in particular, cortisol), insulin, and leptin to promote weight loss. We will provide information regarding how hormones respond to various lifestyle factors which may affect appetite control, hunger, satiety, and weight control. These hormones were not chosen for review because they are the only hormones involved in weight regulation, but rather because together they are well-researched and cover a wide range of physiological functions connected with obesity and weight control. For instance, another hormone of interest in the regulation of body weight is glucagon-like peptide-1 (GLP-1). Exenatide, a GLP-1 receptor agonist, was administered to determine its effects on glycemic control and weight over an 82-week period in patients with type 2 diabetes [2]. At week 30 of the study, the amount of weight lost from baseline was 2.1 ± 0.2 kg compared to 0.3 to 0.9 kg for placebo. Reduction in body weight was progressive, resulting in an average weight loss of 4.4 ± 0.3 kg at week 82 [2].
Key Hormones Involved in Weight Regulation
Ghrelin: The Hunger Hormone
Ghrelin is a 28-amino-acid-residue peptide predominantly secreted by the stomach with substantially lesser amounts being detected in several other tissues [3]. Ghrelin appears in two major forms: acylated and nonacylated ghrelin. Acylated ghrelin is the active form of ghrelin whereas nonacylated ghrelin, which is present in greater quantities than acylated ghrelin, appears to be biologically inactive [3]. Ghrelin is a pleiotropic hormone demonstrating many different roles. Ghrelin displays strong growth hormone releasing activity through the binding to and activation of growth hormone secretagogue receptor type 1a [3]. In addition to growth hormone release, ghrelin stimulates the release of prolactin and adrenocorticotropic hormone, negatively influences the pituitary-gonadal axis, stimulates appetite, influences sleep, controls gastric motility, and modulates pancreas function [3].
Cortisol: The Stress Hormone
Activation of the hypothalamic-pituitary-adrenal axis results in the eventual production of the glucocorticoid known as cortisol [4]. Corticotropin-releasing hormone from the hypothalamus stimulates the release of adrenocorticotropic hormone released from the pituitary gland [4]. Adrenocorticotropic hormone is responsible for the subsequent release of cortisol from the fascicular zone of the adrenal cortex [4]. Cortisol is an adrenal steroid hormone that regulates adaptive responses to varying types of stress [5].
Leptin: The Satiety Hormone
Leptin is a polypeptide hormone product of the ob gene that is produced and secreted by adipocytes [6]. The amount of leptin produced is directly proportionate to the triglyceride content of adipocytes (i.e., the size of the fat cells) [6]. Leptin is a crucial link in the signaling process between changes in body fat and control of energy balance [6].
Insulin: The Blood Sugar Regulator
Insulin is a peptide hormone that is released from the beta cells of the pancreas [7]. Insulin serum concentration increases with feeding and decreases with starvation [7]. Serum insulin levels are most sensitive to changes in blood glucose concentrations. Insulin binds to its receptor to initiate GLUT-4 translocation to the cell membrane in order to allow glucose to enter the cell for energy production and/or storage [7]. Specifically, in this paper, insulin will be investigated in relation to macronutrient composition of meals, meal frequency, exercise, and sleep.
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The Impact of Macronutrient Composition on Hormones and Weight
The macronutrient composition of meals is one variable that may contribute to excessive caloric intake under ad libitum conditions resulting in unwanted weight gain and the onset of obesity. The postprandial endocrine response associated with meals of varying macronutrient proportions may give some insight as to why certain food combinations lead to greater satiety resulting in less caloric ingestion than others. Identifying and exploiting the macronutrient proportions that are associated with satiety and favorable postprandial endocrine responses may be a useful strategy for initiating weight loss through appetite regulation in the absence of purposeful calorie restriction. A majority of the recent studies involving the ingestion of meals of varying macronutrient proportions have focused on the resulting actions of the postprandial ghrelin and insulin response [8-13]. Both exogenous insulin administration and endogenous postprandial insulin response have resulted in suppression of ghrelin [14, 15]. In addition, faulty regulation of ghrelin suppression is associated with insulin resistance [16]. During a euglycemic-hyperinsulinemic clamp procedure, reduction of total and acylated ghrelin was greater in insulin-sensitive overweight and obese individuals versus insulin-resistant individuals of similar body type [16]. Postprandial ghrelin suppression has also been shown to be proportional to meal calorie content, and this association of meal calorie content with ghrelin suppression is reduced in obese individuals [17]. Generally, obese individuals exhibit lower fasting ghrelin levels than their normal-weight counterparts which suggests that it may not be the initial amount of plasma ghrelin that regulates appetite but the magnitude and duration of postprandial ghrelin suppression and its ensuing rise to fasting levels [13, 17].
The fat, protein, and carbohydrate compositions of meals have differing effects on ghrelin suppression as well as appetite regulation and satiety. In one study, high-fat meals (71% energy from fat) led to less ghrelin suppression at 30 minutes post-ingestion when compared to a high-carbohydrate (88% energy from carbohydrates) meal of equal caloric load [13]. In the same study, both lean and obese subjects reported less satiety 30 minutes after the ingestion of the high-fat meal compared with the high-carbohydrate meal. Moreover, Monteleone and colleagues [18] showed similar results in that ingestion of a high-carbohydrate meal (77% energy) more effectively suppressed ghrelin and appetite compared to ingestion of a high-fat meal (75% energy) in nonobese women. In a separate study, Foster-Schubert et al. [9] also demonstrated the inability of fats to effectively suppress postprandial ghrelin concentrations when compared to carbohydrates. In this study, however, no difference in appetite between the macronutrients was reported. Additionally, Kong et al. [11] reported that obese postmenopausal women with higher insulin concentrations had a positive correlation between saturated fat intake and ghrelin levels. Based on the results of these studies, isocalorically increasing the proportion of fat calories in relation to calories from carbohydrates and proteins is not a viable strategy to decrease appetite and ad libitum calorie ingestion.
A study looking at the differences in ghrelin suppression and appetite sensations after either an egg (22% carbohydrate/55% fat/23% protein) or bagel (72% carbohydrate/12% fat/16% protein) breakfast found an inability of either meal to suppress ghrelin [19]. In fact, ghrelin levels were increased after both meals although the rise was significantly less after the egg breakfast. Despite the unexpected increase in ghrelin, the egg breakfast was associated with significantly less “hunger” and greater feelings of satisfaction than the bagel breakfast at three hours after ingestion. Also, consumption of the egg breakfast resulted in a lower overall energy intake compared to consumption of the bagel breakfast during the subsequent 24-hour period. The researchers credited the feelings of satiety associated with consumption of the egg breakfast to the suppressed ghrelin response and tempered insulin/glucose fluctuation [19]. Examination of other research studies suggests that the increased satiety and subsequent decrease in energy intake might be at least partly explained by the higher protein content (23% of calories for egg breakfast versus 16% of calories for bagel breakfast) of the egg breakfast [8, 10, 20]. Specifically, evidence from Leidy et al. [21] supports the idea that a high-protein intake (25% of meal calories from protein) at breakfast may be important for sustained fullness during periods of energy restriction. Conversely, when a high-protein breakfast (58.1% protein, 14.1% carbohydrate) was compared to a high-carbohydrate breakfast (19.3% protein, 47.3% carbohydrate), no difference in subsequent appetite or ad libitum caloric intake during lunch was observed [22]. However, a larger suppression of postprandial ghrelin was observed for the high-protein breakfast [22].
Numerous studies provide evidence that supports the use of a high-protein diet to induce appetite suppression and decreased ad libitum energy intake. Weigle et al. [20] reported that an increase of protein from 15% to 30% of dietary intake resulted in a decrease of ad libitum caloric intake and weight loss. These effects were evident in the absence of ghrelin suppression. Beasley et al. [8] also reported that a meal with 25% protein suppressed appetite (compared to a 15% protein, high-fat group and a 15% protein, high-carbohydrate group). Similar to the results presented by Weigle et al. [20], reduction of appetite could not be explained by a suppression of postprandial ghrelin [8]. The likely mechanism of action of high-protein diets on appetite suppression and decreased caloric intake may be outside of the control of ghrelin.
In addition to a relatively high protein intake (~30% of total calorie intake), moderate carbohydrate intake may also be important in regulating sensations of hunger and calorie ingestion. As mentioned earlier, endogenous insulin secretion may result in the suppression of ghrelin [15]. In a recent study of healthy Pima Indians, higher plasma insulin responses were associated with a decrease in subsequent carbohydrate consumption and less weight gain [23]. These results further point to insulin as a regulator of calorie consumption. While, in one study [24], a short-term isocaloric high-carbohydrate diet was not associated with a lower overall energy intake when compared to a high-fat diet, another study [25] demonstrated that a high-protein meal (35% of total calories) with moderate carbohydrate intake (45% of total calories) was able to persistently suppress ghrelin at levels significantly lower than baseline when compared to either a mixed-diet (50% carbohydrate, 20% protein) or high-fat (45% carbohydrate, 45% fat) meal. It is unclear whether the glycemic index or glycemic load plays a direct role in the regulation of appetite and subsequent energy intake through tempered insulin responses as results from past studies have been conflicting [26, 27]. Furthermore, insoluble fiber at high doses (33-41 grams) may help to regulate appetite as well as energy intake [28, 29]. In conclusion, evidence tends to suggest that for the regulation of ad libitum caloric ingestion, a high-protein diet (~30% of total calories) may be beneficial whereas high-fat diets should most likely be avoided. It would appear to be most beneficial if the additional protein is ingested from solid food sources as food form also appears to play a role in feelings of satiety [30, 31]. Future research should investigate the effects of large doses of insoluble fiber (33 to 41 grams) in addition to a high-protein diet to determine if this combination could further attenuate appetite and energy intake.
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