I. Adipose tissue plays an important role in the maintenance of weight through the release of

The aim of this study revealed an interested trend when comparing IL-6 results to the different metabolic diseases listed as top Ten Global Health Disparities. This study showed that CR will benefit situations where there is a socioeconomic disadvantage, even factor that include health disparities among race and age would show benefit because CR is suitable for all disadvantage groups. Caloric Restriction (CR) has proven to be non-expensive, beneficial agent against age related, racial, and socioeconomic disadvantage, associated with health disparities. The results for IL-6 in each case indicated that CR could improve endothelial function in rats with different metabolic diseases possibly through reduction in body weights resulting in reduction in fat mass and concomitant reduction in the production of the proinflammatory cytokines. IL-6 is expected to be reduced in Colorectal cancer (CRC) rats under

On a molecular level, fat tissue is normally the largest organ in humans and is involved in mechanisms and pathways that deal with longevity. Fat tissue is not only involved in energy storage but is also important in immune and endocrine function, thermoregulation, mechanical protection, and tissue regeneration (Tchkonia et al., 2010). Adipose tissue is able to protect against infection and trauma. It is also able to produce and activate hormones, including IL-6, IGF-1, and glucocorticoids, as well as prevent heat loss (Tchkonia et al., 2010). Throughout life, changes in fat distribution and function is constantly occurring and in older individuals, these changes correspond to a number of health disorders like hypertension, cancers, cognitive dysfunction, and diseases like diabetes, heart attacks, and strokes, as previously noted (Tchkonia et al., 2010). As people age, their body composition increases in fat mass and decreases in muscle mass, regardless of their body weight or BMI (Dorner and Rieder, 2011).

forces the body to dip into its reserve energy stores. In removing fat, however, essential fatty

instrument of the advancement of obesity is not fully recognized and it is understood to be a

     Obesity is the net result of an excess of energy consumption over expenditure. Factors that must be considered as contributing to causation are: heredity, and altered metabolism of adipose tissue, the list goes on and on. Overeating is clearly a prominent contributor to obesity. Feeding behavior occurs in response to hunger and to appetite induced by the presence of food.

Obesity is described by the World Health Organisation (WHO) as unusual or extreme fat growth that presents a risk to a person’s health. Obesity is a complex disease with multiple drivers such as

“ 1. Adipokines are hormones produced by adipose tissue. /…/ Adipokines have effects not only on tissues but [also] on the hypothalamic and pancreatic function. /…/ 2. Elevated serum free fatty acids and high intracellular deposits of triglycerides and cholesterol. These lead to metabolic overload with interfere of insulin signaling and a decrease in tissue response to insulin. 3. Obesity causes release of inflammatory cytokines. /…/ These play an important role in the genesis of a fatty liver [which impairs the function]. 4.

Leptin is released through the arcuate nucleus and leptin helps to check the fat content of the body. If there is not enough fat, then our body gets the signal to be hungry and eat something. There are two types of appetite control neuron in the arcuate nucleus. They are NPY neurons and POMC neurons. NPY neurons can stimulate the appetite and reduce metabolism (Ceballos 2016). When the leptin level is high, this reducing metabolism process can be inhibited. These neurons can work as hunger neurons that can be stimulated by ghrelin. This peptide hormone is made by and released by the gut to increase appetite. During fasting, high concentration of ghrelin can strongly stimulate appetite and decrease suddenly when you eat something. NPY neurons inhibited by PYY3-36 to decrease appetite. PYY3-36 is released by intestinal cells. This small peptide level is increased after a meal to lower the appetite (satiety) signal (Ceballos 2016). This PYY3-36 acts on hypothalamic appetite control mechanism. PYY3-36 is very low in obese people, causing them to feel hungry and gain weight. The other type of appetite control neurons in arcuate nucleus is POMC neurons. These neurons can lower or inhibit appetite and increase the metabolism. They are also useful in acting as satiety

In addition to obesity leading to other health problems, obesity stems from numerous causes such as genetic, environmental, and sociological factors. Other

The relationship between β-oxidation of fatty acids and reactive oxygen species (ROS) production is inversely proportional under normal conditions (6). In type II diabetes, a large amount of reducing equivalents from β-oxidation enter the electron transport chain, diverting complex I where the core ROS production site resides (7,8). An obesity-related disorder such as diabetes causes inflammatory macrophages to invade white adipose tissue, causing inflammation and contributing to insulin resistance (9).

Leptin and ghrelin are internal intermediary that affect feeding and appetite. Ghrelin is secreted by the stomach adjust short-term appetitive control (i.e. to eat when the stomach is empty and to stop when the stomach is filled). Leptin is secreted by white adipose tissue to signal fat storage reserves in the body and mediates long-term appetitive controls (i.e. to eat less when fat storages are high and more when fat storages are low). It plays an efficient role in the regulation of energy balance and body weight by decreaing food intake and stimulating energy expenditure.39 Although, administration of leptin may be effective in a small subset of obese individuals who are leptin deficient. Most obese individuals are thought to be leptin resistant

Strosberg, A. D. and Issad, T. The involvement of leptin in humans revealed by mutations in leptin and leptin receptor genes. Trends Pharmacol. Sci. 6(1), 227-230

Not just a simple hormone, but a very strong one. This hormone basically tells your brain how much fat you have, what to do with it, and also - where to store it. It really tells the brain what to do. That’s why leptin controls appetite, fat-loss, and decides whether you have fat in your belly, hips, or spread evenly all over your

Obesity is a disorder of the Endocrine System. Obesity means having too much body fat, it occurs over time when more calories are eaten than being use. The balance between calories-in and calories-out differs for each person. Factors that might affect weight consist of your genetic makeup, overeating, eating high-fat foods, and not being physically active. Furthermore, several endocrine abnormalities are reported in obesity. Some of these abnormalities are considered as contributory factors for the development of obesity, whereas others are considered to be secondary effects of obesity and usually are restored after weight loss. Thyroid hormones usually are normal in obesity, with the exception of T3 which is elevated. Prolactin is normal but prolactin response to different stimuli is dulled. GH is low and GH response to stimuli is dulled. IGF-I levels are normal or elevated. Cortisol, ACTH, and urine free cortisol levels are usually normal; however, a hyperresponsiveness of the HPA axis with increased cortisol and ACTH response to stimulatory tests is observed in extremely obese individuals.

Incretins, are gut-derived hormones released predominantly by the L cells in the distal bowel in response to a meal. They reduce blood sugar concentrations by enhancing the insulin release from pancreatic beta cells and inhibiting postprandial glucagon secretion and gastric emptying after a meal (Hattori). Ghrelin, a peptide produced by the stomach, stimulates appetite and its levels increase with fasting and decrease after a meal (Cummings). It also has a pro-diabetic role, causing hyperglycemia through inhibition of insulin resistance and stimulation of release of counter-regulatory hormones, and impairing insulin sensitivity (Leite-Moreira). A peptide Obestatin, derived from ghrelin precursor but with opposite effects has recently been found to be produced by the same neuroendocrine cells that secrete the orexigenic hormone but counterbalances its effects by decreasing appetite (Zhang).