Weight Control by Fatimat Adigun-Bello, Dr. Paul Cottrell, Victoria Virgulak and Vivian Okonta.


The word balance is a complicated term in the human life. It is often heard relating to everyday tasks, but often forgotten is the most important balance that of which is found within the human body. One pivotal marker of an individual having balance is having full control of body weight. It is a significant challenge to maintain an ideal fitness and weight. 

The human body has a complex set of hormones and signaling systems that monitor and adjust to retain balance. The systems, if properly maintained, work in harmony. However, if there is a slight issue, the systems can turn on the human body and cause damage. Insulin is able to work in the body as a positive and a negative asset. If properly managed, insulin can assist in weight loss by metabolizing glucose and reducing the need for fat synthesis, however if improperly managed, poor diet can lead to rising levels of insulin and eventually result in weight gain and type II diabetes. To sustain the body’s energy, two important hormones work in opposition of each other - leptin and adiponectin. Leptin suppresses appetite and increases metabolic rate while adiponectin increases appetite and decreases metabolic rate. These hormones exert their actions via other hormones and neuropeptides. Others include ghrelin, neuropeptide Y (NPY) and agouti-related peptide (AgRP) which work together to increase energy intake and promote weight gain. With weight loss, hormones such as ghrelin will increase to guard against continued weight loss. There are several other hormones involved in body weight control that are activated with exercise including testosterone, cortisol, and growth hormone. The duration and intensity of the exercise affects them differently. For example, after an intensive exercise, the body upkeeps the balance by repairing and building muscles via these hormones. 

While there are large strides being made in research on the correct way to balance weight in the human body, there is still research to be done to help combat worldwide obesity and obesity related diseases. There are questions left to be answered, however basic understanding of all the systems and its hormones can progress everyone on the correct path for balance. 


The regulation of body weight and energy homeostasis is controlled by different endocrine systems and metabolic pathways, and food intake is controlled by the CNS through neuroendocrine and neurotransmitter circuits. The involvement of Insulin signaling is mostly done by regulation of energy homeostasis and body weight through its effect on lipid and glucose metabolism [1]. Insulin promotes the storage of glucose and fat and has metabolic effects that determine body weight as an anabolic hormone. 

There are physiological actions of insulin that could have effects on body weight or weight loss in an individual which include the metabolism of macronutrients, cellular growth, stimulation of glucose transport, triglyceride synthesis and inhibiting lipolysis, upregulation of LPL and inhibition of adipocytes HSL through blockage of its phosphorylation [2]. 

In healthy individuals, insulin secretion is exact in meeting the metabolic demand. It binds to a receptor on the plasma membrane and induces secondary messengers in the body. The pancreatic beta cells from the islet of langerhans are stimulated by high levels of plasma glucose and are able to sense change in plasma glucose concentration and act by releasing corresponding amounts of insulin into the blood. Insulin then stimulate cells of the body to uptake glucose. In addition, there are other kinds of hormones that modulate insulin secretion by affecting the timing of its release, one type of hormone is incretins. Incretin is released in the GI tract in response to food intake. Another is GLP (glucagon like peptide 1), a major type of incretin, which provides a feedforward component and further induces the secretion of insulin to glucose overload after taking a meal [4]. In addition, fenestration also modulates insulin secretion and allows for the rapid diffusion into the blood [3]. 

Glucose is the primary stimulus for insulin release, due to its fact that it can accumulate immediately after ingestion of food [3]. Other macromolecules are able to cause secretion of insulin but not in large amounts as glucose. In addition, studies have shown different patterns of food intake within 24 hours of the day or longer which have resulted in decrease or increase of insulin secretion and the effect it has. A study tested glucose and insulin excursions in the response to different meal frequencies and macronutrient composition. The study was done with healthy individuals who ate 6 frequent carbohydrate meals in 12 hours, which resulted in high blood glucose levels over the course of the day, while another group ate 3 carb meals a day and had less blood glucose levels, but both individual groups had no difference in insulin response. They came to a conclusion that different eating patterns during the day may increase blood glucose levels in a course of 24 hours, but there will be no difference in insulin response within 24 hours [5]. Although they were able to see a difference in insulin response over the course of 24 hours, they did not have the same response with different meal frequencies in individuals who had only a protein diet. There was a decrease in insulin response than those individuals. 

There has been the association of obesity and type 2 diabetes for some decades now and the main reason for this link is due to obesity giving rise to insulin resistance (SI) [6]. There is a decrease in the Adipo R expression levels, thereby enhancing insulin resistance in individuals who are obese [2]. Exercise has also been a topic that has been discussed as a way to help reduce obesity and improve glucose homeostasis in individuals. Although, this may seem attractive, this concept is still under intensive research and different strategies are being done in order to get a better understanding of how exercise can be beneficial in obesity. It was concluded that acute exercise enhances glucose uptake but insulin resistance (SI) often sets back to its baseline within a couple of days after the physical activity, leaving the effectiveness of exercise in question [6]. 

On the other hand, some studies have provided evidence that regular intensive physical activity reduces the risk of insulin resistance and type 2 diabetes [7]. Insulin resistance can improve with individuals who comply with exercise on a daily and aerobic exercise interventions can also play a positive part. Individuals with obesity or type 2 diabetes, could benefit on adjusting their lifestyles with proper nutrition and exercise that could favour weight maintenance or loss. In regards to the study previously discussed, a proper nutritional meal that contains more of protein and fat could help with weight maintenance, as it is shown that high protein diets reduce insulin response due to low blood glucose. This adjustment accompanied with physical activity, such as; resistance exercise could improve glycaemic regulations [7] and lead to weight maintenance or loss. 

In conclusion, the study of weight maintenance or loss in obesity has been an ongoing study and having these life nutritional adjustment accompanied with exercise, seem to make a difference in glycaemic regulations. In future studies, Could it be possible to make a change in the decrease in Adipo R expression levels, cause an increase in adiponectin level and decrease insulin resistance in obese individuals? This could stimulate insulin sensitivity which could be beneficial alongside exercise in obese individuals and help with insulin resistance which seems to be the hurdle in obesity and type 2 diabetes. Also, instead of engaging in acute exercise, could the intensity of exercise be longer in time? To make sure SI does not reset back to its baseline as previously discussed. These questionable strategies could benefit weight maintenance over time and create a healthy immune glycemic system. 


1. Dokken, B., & Tsao, T. (2018). The Physiology of Body Weight Regulation: Are We Too Efficient for Our Own Good?. 

2. Singla, P. (2010). Metabolic effects of obesity: A review. World Journal Of Diabetes, 1(3), 76. doi: 10.4239/wjd.v1.i3.76. 

3. Fu, Z., R. Gilbert, E., & Liu, D. (2013). Regulation of Insulin Synthesis and Secretion and Pancreatic Beta-Cell Dysfunction in Diabetes. Current Diabetes Reviews, 9(1), 25-53. doi: 10.2174/157339913804143225. 

4. Kim, W. and Egan, J.M. (2009). The Role of Incretins in Glucose Homeostasis and Diabetes Treatment. Pharmacology Review. 

5. Holmstrup, M., Owens, C., Fairchild, T., & Kanaley, J. (2010). Effect of meal frequency on glucose and insulin excursions over the course of a day. E-SPEN, The European E-Journal Of Clinical Nutrition And Metabolism, 5(6), e277-e280. doi: 10.1016/j.eclnm.2010.10.001. 

6. Kahn, B., & flier, j. (2000). Obesity and insulin resistance. The Journal Of Clinical Investigation, 106(4), 473-481. doi: 10.1172/JCI10842. 

7.  Bird, S., & Hawley, J. (2017). Update on the effects of physical activity on insulin sensitivity in humans. BMJ Open Sport & Exercise Medicine, 2(1), e000143. doi: 10.1136/bmjsem-2016-000143. 

Leptin and Adiponectin

Leptin regulates energy balance by inhibiting hunger through opposition to the actions of the hormone ghrelin. Adiponectin are involved in regulating glucose levels and fatty acid breakdown. 

To maintain long-term energy homeostasis leptin expression and secretion are elevated during energy absorption [1]. When energy intake exceeds energy expenditures fat deposition results, which releases higher levels of leptin into the plasma. Leptin then signals the hypothalamus to inhibit hunger through the neurotransmitter neuropeptide Y and suppression of ghrelin hormones. This inhibition of hunger signal from leptin lowers energy intake and increases metabolic rate. This negative feedback loop in extremely important in long-term maintenance of the energy intake and energy expenditure balance. The short-term effects of higher plasma levels of leptin are to suppress hunger, which helps to control insulin secretion during absorption episodes—reducing glucose uptake by cells. 

To maintain long-term energy homeostasis adiponectin is secreted from adipocytes, which is also known to have antidiabetic, antiatherogenic, anti-inflammatory, and angiogenic properties [2]. A short- term effect of adiponectin secretion is the effects on muscle tissue, whereby it stimulates glucose transport by increasing GLUT4 translocation—leading to increased energy expenditures [2]. Another short-term effect of adiponectin secretion into plasma is to lower the production of glucose from hepatic cells [3]. In normal individuals, to maintain glucose and fatty acid levels adiponectin is a negative feedback on glucose production and a positive feedback on fatty acid oxidation. 

Obesity and metabolic syndrome have been linked to hypothalamic-pituitary-adrenal axis dysfunction and local metabolism of glucocorticoids in adipose tissue [4]. Adiponectin receptors are present in human adrenals and that glucocorticoids and ACTH are known to decrease adiponectin production in white adipose tissue [4]. 

There is an inverse relationship with adiponectin production and amount of adipose tissue, whereas there is a positive correlation with leptin production and the amount of adipose tissue. These relationships allow for setting a lower bound and upper bound in weight fluctuation, e.g. leptin sets upper bound and adiponectin sets lower bound. Unfortunately resetting boundaries upward is easier for most people than to resetting a downward direction. These resetting phenomena might be evolutionary to maintain energy balance biased to the higher weight setpoint. This prevents overweight individuals from losing weight on a permanent basis. It has been found that leptin-infused mice do not subsequently defend a higher body weight after infusion [5]. 

To promote weight loss, it is hypothesized lipolysis would need to be increased. This increase in lipolysis could be through increased cortisol levels, anti-inflammatory signaling, increased leptin and lower adiponectin signaling. Since the body has reset points for leptin and adiponectin based on the amount of adipose tissue and CNS sensitivity to leptin, a long-term lifestyle change would be needed to properly reset upper and lower bound limits of energy balance. One possible lifestyle change that would affect the endocrine system related to leptin and adiponectin would be a slow reduction in caloric intake. By phasing caloric restriction slowly, the glucose levels are lower leading to lipolysis and gluconeogenesis long-term. This will in turn lead to reduced fat cells over a sustained timeframe and a chance for the CNS to up-regulate leptin sensitivity. Also, to increase energy expenditures during the calorie restriction phase a mild exercise regime would maintain IL-6 plasma levels, inhibiting protein breakdown and maintaining musculature. The mild exercise regime should decrease after the weight target has been reached and maintained for one year. This deduction in exercise and maintained caloric levels further establishes the reset point for energy balance. 

To promote weight gain, it is hypothesized one would need to reset the upper bounds of
leptin. This is accomplished through extensive exercise to increase muscle mass and a phased-in caloric increase. Positive energy balance will activate insulin to store the excess of glucose into cells for storage. This will also overtime lead to lower sensitivity to leptin in the CNS to reduce hunger inhibition. After the weight target has been reached exercise regime should be mild to keep musculature and caloric intake should be slightly reduced to reinforce the upper bound reset point for energy balance. 

Additional research in long-term resetting upper and lower bound energy balance limits are required to further formulate lifestyle recommendations for sustained weight loss and gain. Two follow- up research questions are: (a) How the CNS sensitivity for leptin changes long-term in anorexia nervosa patients with a slow increased caloric intake regime, and (b) How the CNS sensitivity for leptin changes long-term in obese patients with a slow decrease in caloric intake regime? 


1. Menzbert, H., & Morrison, C. D. (2015). Structure, production and signaling of leptin. Metabolism, 64(1). 13-23. doi:10.1016/j.metabol.2014.09.010

2. Dos Santos, E., Pecquery, R., de Mazancourt, P., & Dieudonné, M. (2012). Adiponectin and Reproduction. Vitamins and Hormones, 90.187-209. http://dx.doi.org/10.1016/B978-0-12-398313- 8.00008-7 

3. Fiaschi, T., Magherini, F., Gamberi, T., Modesti, P.A., & Modesti, A. (2014). Adiponectin as a tissue regenerating hormone: more than a metabolic function. Cellular and Molecular Life Sciences, 71. 1917- 1925. doi:10.1007/s00018-013-1537-4

4. Kargi, A.Y., & Iacobellis, G. (2014). Adipose tissue and adrenal glands: novel pathophysiological mechanisms and clinical applications. International Journal of Endocrinology, 2014. 1-8. http://dx.doi.org/10.1155/2014/614074 

5. Ravussin, Y., LeDuc, C. A., Watanabe, K., Mueller, B. R., Skowronski, A., Rosenbaum, M., & Leibel, R. L. (2014). Effects of chronic leptin infusion on subsequent body weight and composition in mice: can body weight set point be reset? Molecular Metabolism 3, 432-
440. http://dx.doi.org/10.10.16/j.molmet.2014.02.003 

Neutopeptide Y, Gherkin and Agouti-related Peptide

Ghrelin, neuropeptide Y (NPY) and agouti-related peptide (AgRP) work together to increase energy intake and reduce energy expenditure which can ultimately result in weight gain (1,2). Ghrelin is primarily secreted by enteroendocrine cells in the stomach and other areas in the body such as the hypothalamus and pancreas. In response to hunger, when the stomach is empty and glucose levels are low, ghrelin is secreted in high amounts. Ghrelin activates growth hormone secretagogue receptors (GHSR) in the ARC nucleus to increase the synthesis and release of NPY and AgRP. These neuropeptides then increase appetite. In addition, ghrelin stimulates stomach motility, acid secretion and growth hormone secretion. Together, ghrelin and NPY increase lipogenesis and gluconeogenesis. On its own, NPY suppresses sympathetic nervous system (SNS) activity and decreases metabolic rate via suppression of the hypothalamic-pituitary-thyroid axis. These actions combined move the body towards a positive energy balance. (1–3) 

Normally, ghrelin levels rise during periods of fasting and fall soon after a meal is consumed but genetic mutations can also play a role in its secretion and activity (3). Ghrelin is a polypeptide in which several polymorphisms can exist predisposing an individual to have higher or lower total ghrelin levels. For example, the Arg51Gln is a single nucleotide polymorphism (SNP) that interrupts the normal production of a mature ghrelin peptide. Studies have shown that those with the Arg51Gln mutation have lower total levels of circulating ghrelin. (3,4) Genetics also play a role in the dysfunctional secretion of ghrelin in individuals with Prader-Willi Syndrome but the exact mutation is not yet known. This genetic disorder is characterized by hypotonia and poor feeding at birth followed by hyperphagia and excessive weight gain. When looking at a group of PWS individuals, ghrelin levels are constantly high throughout their lifetime and suspected to be the cause for hyperphagia (5). Lastly, several studies have been done looking at the ghrelin levels of individuals with eating disorders such as anorexia nervosa (AN). Individuals with AN have been found to have higher levels of fasting ghrelin compared to healthy normal weight controls (3). However, more research needs to be done to determine whether there are genetic factors at play or if the altered ghrelin levels are a result of prolonged starvation and the underweight status of those with AN. 

Several lifestyle patterns have been suggested to decrease the secretion of these hormones and promote weight loss. Schmid et al. suggest that adequate sleep can lead to lower levels of ghrelin. Additionally, high protein and keto diets lead to lower levels of post-meal and total circulating ghrelin levels. Blom et al. showed that individuals who had a high protein meal suppressed ghrelin levels stronger than those that had a high carbohydrate meal. This greater suppression of ghrelin reduced appetite and energy intake during the next meal (6). An individual may also opt to use a keto or high fat, low carb diet to attenuate the increase in ghrelin that comes with weight loss. The increase in ghrelin that comes with weight loss is the body’s effort to maintain homeostatic weight by intensifying triggers for food intake. Thus, in order to keep the weight off, individuals may adapt ways to minimize the normal elevation of ghrelin that comes with weight loss. Findings from a study by Sumi et al. found that participants who lost weight on a keto diet did not have as a significant increase in fasting plasma ghrelin compared to participants on a high carb, low fat diet. Fat has also been hypothesized to better signal to the hypothalamus that there is enough food around and decrease the expression of NPY (7). Furthermore, specific types and doses of exercise can have different effects on ghrelin levels. Fasting ghrelin levels are shown to decrease more with moderate-dose (14 kcal/kg per week) exercise as opposed to low-dose (8 kcal/kg per week) (8). Therefore, a high protein or high fat diet combined with proper sleep and moderate dose exercise may promote weight loss and maintenance. 

On the contrary, any lifestyle patterns that would increase the secretion or action of these hormones may also promote weight gain. Just one night of sleep restricted to 4 hours leads to increased total ghrelin levels and appetite (9). Meals containing high fructose content decrease ghrelin levels to a lesser degree (10). Therefore, poor sleep, low dose exercise and diet consisting of high carbohydrates and fructose can increase ghrelin secretion and action via NPY and AgRP ultimately resulting in increased appetite, food intake and weight gain. 

There are still a myriad of unanswered questions pertaining to how the manipulation of ghrelin, NPY and AgRP can effectively promote weight gain and loss. The recommendations described are mostly based on data involving persons that are of normal weight. Is it possible for those that are already overweight or obese to adapt these lifestyle patterns and exert similar effects on these hormones? Furthermore, these data describe lifestyle changes adapted for short periods of time. More research is needed to determine if the effects on ghrelin can be maintained long-term. Are the changes in ghrelin in response to the adapted lifestyle patterns just temporary? 

1. Ibrahim Abdalla MM. Ghrelin – Physiological Functions and Regulation. Eur Endocrinol. 2015 Aug;11(2):90–5. 

2. Delporte C. Structure and Physiological Actions of Ghrelin [Internet]. Scientifica. 2013 [cited 2018 Oct 18]. Available from: https://www.hindawi.com/journals/scientifica/2013/518909/ 

3. Ando T. Chapter Four - Ghrelin Gene Variants and Eating Disorders. In: Litwack G, editor. Vitamins & Hormones [Internet]. Academic Press; 2013 [cited 2018 Dec 2]. p. 107–23. (Anorexia; vol. 92). Available from: http://www.sciencedirect.com/science/article/pii/B9780124104730000040 

4. Ukkola O, Ravussin E, Jacobson P, Pérusse L, Rankinen T, Tschöp M, et al. Role of Ghrelin Polymorphisms in Obesity Based on Three Different Studies. Obes Res. 2002 Aug 1;10(8):782–91. 

5. Atalayer D, Gibson C, Konopacka A, Geliebter A. Ghrelin and Eating Disorders. Prog Neuropsychopharmacol Biol Psychiatry. 2013 Jan 10;40:70–82. 

6. Blom WA, Lluch A, Stafleu A, Vinoy S, Holst JJ, Schaafsma G, et al. Effect of a high-protein breakfast on the postprandial ghrelin response. Am J Clin Nutr. 2006 Feb 1;83(2):211–20. 

7. Sumithran P, Prendergast LA, Delbridge E, Purcell K, Shulkes A, Kriketos A, et al. Ketosis and appetite-mediating nutrients and hormones after weight loss. Eur J Clin Nutr. 2013 Jul;67(7):759–64. 

8. Bowyer KP, Carson JA, Davis JM, Wang X. The influence of exercise training dose on fasting acylated ghrelin concentration in older women. J Behav Med [Internet]. 2018 Nov 17 [cited 2018 Nov 29]; Available from: https://doi.org/10.1007/s10865-018-9990-z 

9. Schmid SM, Hallschmid M, Jauch‐Chara K, Born J, Schultes B. A single night of sleep deprivation increases ghrelin levels and feelings of hunger in normal-weight healthy men. J Sleep Res. 2008 Sep 1;17(3):331–4. 

10. Teff KL, Elliott SS, Tschöp M, Kieffer TJ, Rader D, Heiman M, et al. Dietary Fructose Reduces Circulating Insulin and Leptin, Attenuates Postprandial Suppression of Ghrelin, and Increases Triglycerides in Women. J Clin Endocrinol Metab. 2004 Jun 1;89(6):2963–72. 


The human body is a complex mechanism that has an intricate system of hormones maintaining and monitoring to upkeep a healthy system. The science behind maintaining a healthy body has been debated and updated over the course of history, from dictating what to eat or how to exercise. Hormones such as neuropeptide Y, ghrelin and agouti-related peptide control appetite that in return control food intakes, which affects weight gain or loss. Besides food intake, exercise plays an important role in sustaining a healthy human body. Exercise produces hormones such as testosterone, cortisol, and growth hormone and yields myokines secretion, which assists in muscle building and recovery. The human body has to maintain a balance with exercise, which causes metabolic changes. The essential focus is preserving a fit and healthy body by triggering the intricate system of hormones working cohesively 

Exercise in the body triggers three important hormones, testosterone, cortisol, and growth hormone. Testosterone is increased in the body during and after workouts, which helps with muscle repair. When there is a moderate to high intensity exercise, it has been shown that there is a great elevation in testosterone [3]. Cortisol provides energy while the body is in exercise status and also assists in anti-inflammatory response. Cortisol levels are highly elevated like testosterone when there is high intensity workout and 24 hours after [3]. Low intensity workouts do not “result in significant increases in circulating cortisol levels” [2]. There is strong research supporting that like testosterone and cortisol, growth hormone’s response is produced by high intensity workouts. There is research that shows that the sex of the human plays a key factor. In young women, growth hormone response occurs due to the intensity, while for young men the growth hormone response occurs due to the duration [7]. Humans that are older or unfit have shown that growth hormone secretion is decreased. Exercise is a good indicator to stimulate growth hormone in the body [8].  The intensity and duration of exercise is quite important to the human body for the stimulation of hormones. 

While triggering exercise hormones, a workout also triggers appetite hormones, ghrelin is suppressed during workout and increased after a workout. Leptin is increased during exercise to decrease appetite, after exercise, it decreases to up the food intake. 

Hormones are not the only mechanism that is activated during exercise in the body; myokines are secreted in the muscles. The myokines regulate anti- inflammation in the body after exercise. There are different types of myokines that present themselves around in the body after period a of exercise. Some myokines are considered as a exercise factor like, ANGPTL4, CCL2, and many more, however, there is more research needed to see the effects on the body. There is little data available for each individual myokine that investigates the effects of duration and intensity of exercise in the human body. For example, IL-6 has been showing to be present in high levels during a short form of exercise, however during moderate exercise the concertation plummets [1].  Each myokine has a potential to influence the human body in different ways during and after exercise, while myokines play a role in the body metabolism is also effected from exercise. 

Metabolism is modified during continuous exercise. Professor Herman Pontzer’s research describes that no matter the physical activity of all humans, they all expend the same amount of calories. The common belief is that the greater the physical activity done, the greater benefit is found to the human body, however the belief is not accurate and proves to have negative effects [6].  Current health suggestions should be reformatted to adapt Pontzer’s research, “expenditure and the complex effects of physical activity on metabolic physiology. to better reflect the constrained nature of total energy” [4]. The idea of  maintaining a healthy body is to work smarter, not harder.

A person who is motivated or less motivated to workout, both should be able to workout with a similar regime, given that they are the same sex such as women. They should follow a schedule of  exercising a few times a week to activate exercise hormones by working out high intensity workouts to maintain healthy body weight. However, it would all depend on their starting shape, there is still researched needed to determine, would a better understanding of myokines change an exercise regime or would additional growth hormone supplements promote weight loss or weight maintenance? 


1. Catoire, M., & Kersten, S. (2015, May). The search for exercise factors in humans. Retrieved from 


2. Hill, E. E., Zack, E., Battaglini, C., Viru, M., Viru, A., & Hackney, A. C. (2008, July). Exercise and 

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(2016, February 08). Constrained Total Energy Expenditure and Metabolic Adaptation to Physical 

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Retrieved from https://www.sciencedirect.com/science/article/pii/S0960982215015572#bib3 

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December). The impact of sex and exercise duration on growth hormone secretion. Retrieved from 


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Growth Hormone Release During Acute and Chronic Aerobic and Resistance Exercise. Retrieved from 



Weight management involves complex process in the endocrine system. In this paper we explore the effects of many systems: (a) insulin, (b) leptin and adiponectin, (c) neuropeptide Y, (d) ghrelin, (e) agouti-related peptide, and (f) exercise. 

In terms of insulin, weight management can be achieved through having a high protein diet, which will cause less insulin response in the system along with regular intensive physical activity to help reduce the risk of insulin resistance and type 2 diabetes in obese individuals. Physical activity should be done in longer durations than acute, as to keep a steady weight if one decides to stop exercising or slow down and to also balance the baseline of insulin sensitivity in obesity. 

Within the leptin and adiponectin paradigm weight management is possible. One possible lifestyle change that would affect the endocrine system related to leptin and adiponectin would be a slow reduction in caloric intake. By phasing caloric restriction slowly, the glucose levels are lower leading to lipolysis and gluconeogenesis long-term. This will in turn lead to reduced fat cells over a sustained timeframe and a chance for the CNS to up-regulate leptin sensitivity. Also, to increase energy expenditures during the calorie restriction phase a mild exercise regime would inhibit protein breakdown and maintaining musculature. The mild exercise regime should decrease after the weight target has been reached and maintained for one year. 

Within the neuropeptide Y, ghrelin and agouti-related peptide paradigm weight loss can be achieved through moderate exercise that expends 14 kcal/kg/wk. Consumption of a high protein, high fat and low carbohydrate diet is recommended. This regimen will decrease ghrelin, neuropeptide Y and agouti-related peptides which will decrease appetite and food intake—leading to weight loss. 

Research has shown the idea is to workout smarter, not harder. High intensity over a short period of time provide better results in activating all hormones to build and recover muscles. Maintenance of weight have been found difficult for many individuals, therefore exercise alone is not a prescribed treatment for sustained weight loss and treatment needs to be coupled with other paradigms represented in figure 1 below.