Craving for Food or overeating.
We, humans turn the excess carbohydrate we eat into fatty acids (and this is a so-called metabolic one-way-street: once you turn carbohydrate into fat, you can’t turn it back into glucose again)and ends ultimately up as triglyceride in our fat cells.
Your body turns excess glucose into fat (technically, turn acetyl-CoA into malonyl-CoA into palmitate), and you can't turn that fat back into glycogen. The increasing use and shift toward more carbohydrates has resulted in the obesity crisis. Not fat makes fat but the hydrocarbons, there might others adding to it but this is the main reason. Its main function is to be a reserve of lipids, which can be burned to meet the energy needs of the body and to protect it from excess glucose by storing triglycerides produced by the liver from sugars, although some evidence suggests that most lipid synthesis from carbohydrates occurs in the adipose tissue itself. Adipose depots in different parts of the body have different biochemical profiles. Under normal conditions, it provides feedback for hunger and diet to the brain.
Eating glucose/sugars (carbohydrates) increases insulin levels in our body. Insulin drives glucose into liver and muscle cells as glycogen (in small, finite amounts) and into fat cells as triglycerides (in unlimited amounts). Insulin also inhibits the breakdown and utilization of stored fat. Parenthetically, this means no one disputes it. With increasing numbers of rings – "complexity" – these saccharides take on broader names like oligosaccharides and polysaccharides. The complexity is often inversely correlated with how quickly they lead to a rise (and fall) in blood glucose levels. In other words, it’s usually the case that the more simple (i.e., smaller) a carbohydrate, the quicker it gets into the bloodstream, and the quicker it elicits an insulin response.
If this sounds crazy – the notion that insulin plays such a crucial role in fat tissue — consider the following two clinical extremes: type 1 diabetes (T1D) and insulinoma. In the former, the immune system destroys beta-cells (the pancreatic cells that make insulin) – this is an extreme case of low insulin. In the case of the latter, a tumour of the beta-cell leads to hyper secretion of insulin – this is an extreme case of high insulin. Prior to the discovery of insulin as the only treatment, patients who developed T1D would become emaciated, if the other complications of glycosuria and dehydration didn’t harm them first. They literally lost all fat and muscle. Conversely, patients with insulinoma often present looking not just obese, but almost disfigured in their adiposity. As these tumours were removed the patients would begin to return to their previous state and the adipose tissue would melt away.
Obesity is multifactorial; its causes include both excess energy intake and inadequate energy expenditure. A great deal of controversy exists about the role of dietary carbohydrate and fat in contributing to obesity. Current dietary guidelines focus on lowering dietary fat and increasing carbohydrate intake.
Americans have steadily reduced their reported intake of dietary fat, yet we are in the midst of a national epidemic of obesity. The prevalence of obesity has risen progressively from the mid-1970s to the mid-1990s, and over 50% of Americans are overweight, defined as a body mass index greater than 25 kg/m2. These statistics suggest that the cause of obesity is probably not related to consumption of dietary fat as suggested.
In theory, the stimulatory effect of increased carbohydrate intake (especially sugar or processed carbohydrates) on insulin concentrations provides a sound biological mechanism linking high-glycemic carbohydrate diets to weight gain, given the potent antilipolytic effects of insulin at physiologic concentrations.
Very-low-carbohydrate diets result in lower insulin concentrations, in addition to suppressing appetite, both of which could enhance long-term weight loss and weight maintenance.
Scientific and anecdotal evidence clearly indicate that very-low-carbohydrate diets reduce appetite and caloric intake. This may be partially due to the fewer food choices available on the diet, but a more likely explanation is the higher satiety value of fat and protein or the anorectic effect of ketosis.
Increased circulating levels of beta-hydroxybutyrate (the primary ketone in the blood) act as a satiety signal.
Given that most people who lose weight find it difficult to keep the weight off, the high level of appetite satiation associated with very-low-carbohydrate diets could enhance successful adherence to a long-term low-energy diet. A very-low-carbohydrate diet can include a wide range of vegetables (eg, tomatoes, cucumbers, peppers) and even small amounts of fruit. It would also be prudent to take a multivitamin/mineral supplement to ensure adequate intakes of all essential micronutrients.
"Kenny and graduate student Paul Johnson focussed on a docking point, or receptor, on the surface of neurons that binds to a "feel-good" brain chemical called dopamine. Dopamine is released by pleasurable experiences such as sex, food and narcotics."These findings confirm what we and many others have suspected, that overconsumption of highly pleasurable food triggers addiction-like, neuroadaptive responses in brain reward circuitries, driving the development of compulsive eating," says Kenny.
The research, based on lab animals, bolsters long-standing suspicions that addiction to pleasure stems from over stimulus of a key reward mechanism in the brain, its authors say. "Common mechanisms may therefore underlie obesity and drug addiction." The research has yet to be conducted among humans.
Obesity is a multifactorial disease characterized by an excessive weight for height due to an enlarged fat deposition such as adipose tissue, which is attributed to a higher calorie intake than the energy expenditure. The key strategy to combat obesity is to prevent chronic positive impairments in the energy equation. However, it is often difficult to maintain energy balance, because many available foods are high-energy yielding, which is usually accompanied by low levels of physical activity. The pharmaceutical industry has invested many efforts in producing ant obesity drugs; but only a lipid digestion inhibitor obtained from an actino-bacterium is currently approved and authorized in Europe for obesity treatment. This compound inhibits the activity of pancreatic lipase, which is one of the enzymes involved in fat digestion. In a similar way, hundreds of extracts are currently being isolated from plants, fungi, algae, or bacteria and screened for their potential inhibition of pancreatic lipase activity. Among them, extracts isolated from common foodstuffs such as tea, soybean, ginseng, yerba mate, peanut, apple, or grapevine have been reported. Some of them are polyphenols and saponins with an inhibitory effect on pancreatic lipase activity, which could be applied in the management of the obesity epidemic.
In humans, adipose (fat or lipids holding)tissue is located beneath the skin (subcutaneous fat), located around internal organs (visceral fat), in bone marrow (yellow bone marrow) and in the breast tissue. Adipose tissue is found in specific locations, which are referred to as adipose depots. Apart from adipocytes, which comprise the highest percentage of cells within adipose tissue, other cell types are present, collectively termed stromal vascular fraction (SVF) of cells. SVF includes preadipocytes, fibroblasts, adipose tissue macrophages, and endothelial cells. Adipose tissue contains many small blood vessels. In the integumentary system, which includes the skin, it accumulates in the deepest level, the subcutaneous layer, providing insulation from heat and cold.
Around organs, it provides protective padding. However, Important questions need to be addressed concerning the advantages and disadvantages of very-low-carbohydrate diets. Hard data are limited but suggest that these diets are not harmful in the short term and may have therapeutic value for weight loss and certain other medical conditions.
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