WAT Utilitarianism

Towards the end of his medical training in the early 1980s, Gokhan Hotamisligil was working on a unique tumor case on a patient and found they were comprised primarily of fat cells. The fatty tumors were due to a rare condition, Proteus Syndrome. Working in the field of metabolic regulation Hotamisligil began to explore the underlying pathways for insulin resistance. In his dissertation he discovered that the fat tissue of obese animals and humans were capable of producing inflammatory mediators. His research helped shape the current view of fat tissue as a “discrete, active organ in its own right, continuously exchanging messages with the rest of the body by way of the bloodstream.” By early 2002 Hotamisligil and his laboratory made

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).

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

When there is an increase in blood glucose, the beta cells detect this change and respond instantly by releasing stored insulin while rapidly producing more, vice-versa when low blood sugar levels are detected. When blood glucose levels decrease, the alpha cells also detect this change and also respond by instantly releasing glucagon and rapidly producing more of the hormone. The adrenal gland secretes a number of hormones that regulate a balance between the process of blood glucose that enters and leaves the blood which maintains a stable blood glucose level. One of these hormones is epinephrine, also known as adrenaline is secreted by the medulla of the adrenal glands. Epinephrine can be released into the bloodstream, resulting in an increase in glucose metabolism. This reaction known as “fight or flight” ultimately prepares the body for intense activity. The effectors of this mechanism is the liver that is referred to on the model, adipose tissue and the skeletal muscles. The diagram shows that the liver both stores glycogen and produces glucose, helping the blood glucose levels to remain constant. It produces glucose by the breakdown of poly saccharide glycogen that is stored in the liver cells. These liver cells

Ghrelin is initially synthesized as a pre-prohormone comprised of 117 amino acids. Cleavage of preproghrelin results in two mature ghrelin molecules. Ghrelin is a 28-amino acid peptide that is secreted primarily from the X/A-like cells of the stomach. Ghrelin is found in blood circulation in two forms, both des-acl (dAG) and acyl forms (AG). Ghrelin is stimulator of growth hormone (GH) secretion and the only circulatory hormone known to significantly enhance feeding, increase body mass and to regulate energy homeostasis central systemic administration (Castañeda et al., 2010; Scerif, Goldstone and Korbonits, 2011; Heppner and Tong, 2014).

Over two thirds of US adults are overweight or obese22 generating an estimated health care cost of $150 billion2. Obesity is one of the major risk factors for development of type 2 diabetes, cardiovascular disease, and cancer23. Energy homeostasis relies on an intricate balance between energy intake and expenditure and disruption in this balance can result in obesity. Feeding is a complex behavior and is largely regulated by two systems. Feeding to maintain metabolic needs, or homeostatic feeding, is regulated by homeostatic feeding circuits, whereas reward-based intake of palatable food, such as foods rich in fat and sugar, is regulated by the mesolimbic DA system23,24. The two systems are not autonomous, however. Energy deficit

The catecholamines consist of norepinephrine and epinephrine, and their role is activate B-adrenergic receptors (βARs) to increase cAMP levels and cAMP-dependent protein kinase A (PKA) activity. This phosphorylation stimulates the release of adipose energy stores due to lipolysis (the hydrolysis of triglycerides) and the liberation of free fatty acids. Insulin is the opposing metabolic regulator that antagonizes the action of catecholamines to stimulate lipolysis by activating phosphodiesterases that degrade cAMP and by using the protein kinase AKT to activate lipid synthesis pathways to promote energy

The leptin hormone is derived from adipose (fat) tissues. This circulating hormone is used to communicate to the central nervous system (CNS) and indicates whether the body has enough energy present. When there is enough energy, leptin communicates to the body that it is full; signaling to the body that it no longer needs to nourish itself. When there is enough energy present and no food intake, the body then utilizes and expends the energy that is presently stored. In this research paper, I will briefly cover the pathway of a normally functioning leptin; as well as the mechanism of leptin resistance, and research is provided to elaborate.

These 3T3-L1 cells are capable of differentiating from fibroblasts into adipocytes under certain conditions. 3T3-L1 cells are classified as Biosafety Level 1 [2]. 3T3-L1 cells divide rapidly until they reach 100 percent confluency, which primes them to differentiate into adipocytes. The purpose of this study was to examine 3T3-L1 cells before and after differentiation to compare their morphology and lipid content.

This design is intended for us to maintain normal, healthy weight. Our lifestyle choices can either allow us to maintain normal weight or cause us to get out of sync. For example, if you do not have adequate sleep you will create more ghrelin and less leptin. This will result in an increase in appetite and reduce the burning of calories. Another example is when you reduce your food intake when dieting; ghrelin production is increased. This increase sends a signal to your hypothalamus that you need to eat more. It is this lack of sleep that forces your body to work against itself and not maintain and optimal environment for a healthy weight.

Illustrated model of adipokine-endothelial cell interaction. Adipocytes generates many hormones and cytokines such as TNF-α, PAI-1, leptin, adiponectin, and resistin. These factors have a main role in adipose tissue, and act locally. They also are important in cell signaling, and have significant effects as circulating bioactive factors. Resistin directly stimulates the activation of endothelial and modulates endothelial function, so this represents resistin is an important link between insulin resistance and cardiovascular

Smartphones and digital devices have become an essential part of everyone. These devices can be used for communication, information searching and entertainment anywhere, anytime. In spite of their favourable capabilities, recent MIT’s report concluded that usage of these devices in class negatively affect student’s academic performance (Carter). Hence, RUX University decided to install cellphone jammer and restrict Wi-Fi access on campus. Kantianism, Act Utilitarianism, Rule Utilitarianism and Social Contract theories will help evaluate the justification of this action.

Adipocytes in human white adipose tissues can change from white to brown and oppositely .Fat is mostly stored in white adipose tissue (WAT). Brown adipose tissue (BAT) is additional fat storage, which in contrast to white adipose tissue is capable to produce heat and preserve body temperature. Brown adipocytes are located in the brown adipose tissue and smaller populations were recognized within white adipose tissue. Brown adipose tissue developed in mammals to dissipate large amounts of biochemical energy in form of heat for protection from the cold. Upon cold exposure, brown adipose tissue is activated by central nervous system (CNS) mechanisms over and done with the sympathetic nervous system(160). 160

Leptin is a hormone produced by the fat cell (adipocytes), the ob gene encodes it and its function is to control the brain (hypothalamus) to inhibit food intake and increase energy expenditure

Adipose tissue is the specialized connective tissue which stores energy as fat, as well as being responsible for generating heat within the body (9). The two types of adipose tissue, white adipose tissue (WAT) and brown adipose tissue (BAT), have distinct roles in fat storage and obesity. BAT is a major source of thermogenesis, and its development has been implicated in suppressing diet induced obesity (9). The brown adipocytes which make-up BAT contain many mitochondria and express high levels of uncoupling protein-1 (UCP1), a protein which generates heat through uncoupling of the respiratory chain and substrate oxidation (11). WAT performs the anabolic role of storing energy, and has been linked to diseases such as type 2 diabetes in states of prolonged obesity (1,9). More recently however, an additional subcategory of adipocytes has been discovered, known as beige or brite (brown in white) adipocytes. These cells are similar to brown adipocytes as they express high levels of UCP1 and stimulate thermogenesis, however their presence in WAT can induce lipolysis of WAT stored fat (7,17). This WAT browning pathway is an area of active research, as the energy expenditure presents a potential strategy for treating obesity. The differentiation of brite adipocytes is unknown however, as