User:Anthony Salvagno/Notebook/Research/2009/08/11/Learning About Fat Cells

Human fat cells that is...

I am reading this to see if there is any way to combine my infatuation with weight loss and possible research in the field to which we can get funded for.

Intro (Wikipedia Read)

The primary fat cell in the human body, that we associate with fat (obesity, etc), is called an adipocyte. Specifically it would be a white fat cell or unilocular. Here is the excerpt from Wikipedia:

White fat cells or monovacuolar cells contain a large lipid droplet surrounded by a layer of cytoplasm. The nucleus is flattened and located on the periphery. A typical fat cell is 0.1mm in diameter with some being twice that size and others half that size. The fat stored is in a semi-liquid state, and is composed primarily of triglycerides and cholesteryl ester. White fat cells secrete resistin, adiponectin, and leptin. An average adult has 30 billion fat cells with a weight of 30 lbs or 13.5 kg. If excess weight is gained as an adult, fat cells increase in size about fourfold before dividing and increasing the absolute number of fat cells present.

Paper: Obesity and the role of adipose tissue in inflammation and metabolism

Author: Andrew S Greenberg and Martin S Obin

I'm reading this paper for some background and references which may point me towards more background.

In a discussion about the health of a subject with regards to the fat cells, the paper discusses a study done where a mouse was genetically altered to have no white fat cells (wfc) and as a result had severe health problems. They then transplanted wfcs from a healthy mouse into the no fat mouse and his symptoms changed. This makes me wonder whether people with liposuction will begin to have adverse affects from the procedure in a short time (assuming this procedure began in the last 15-20 years).

Adiponectin is a protein produced in vast quantities in fat cells. Apparently it plays a large role in insulin sensitivity. Leptin is another protein from fat and influences food intake. These proteins, along with many others discovered recently, give rise to the belief that fat is an organ all its own. From the article:

In humans, plasma adiponectin concentrations fall with increasing obesity, and this effect is greater in men than in women (8). Reduced adiponectin concentrations correlate with insulin resistance and hyperinsulinemia (9, 10). In addition, several polymorphisms of the adiponectin gene (APM1, mapped to chromosome 3q27) have been identified that are associated with reduced plasma adiponectin concentration (11-13) and that increase the risk of type 2 diabetes, insulin resistance, or the metabolic syndrome (11, 12, 14).

Looks promising in correlation with DNA unzipping and Alternative Splicing. I don't know how yet, but more reading will help.

Leptin is pretty interesting itself. As I understand it, leptin controls the intake of food. In mutations preventing the production of leptin, subjects ate more and then got fat. Also the receptor for this protein could be inhibited and the same result would happen. But in obese individuals, leptin was in high concentrations indicating that as more leptin is produced to regain control, target cells would become resistant to the protein. In those cells, SOCS-3 (suppressor-of-cytokine-signaling) was found to be in increased production. SOCS-3, of course, is an inhibitor of leptin.

Side Note: I had to look up the function of insulin because it was talked about so much here. I found out that it is a hormone that enables cells to absorb glucose from the blood stream to get the energy it provides. Insulin deficiency is Type1 diabetes, and Insulin resistance is Type2, both suck. End Note

Being obese increases a fat cells production of free fatty acids which in turns increases insulin resistance in cells that need it. Another major player is the increase of macrophages which scavenge for dead or nearly dead adipocytes (fat cells). The presence of macrophages induces the production of inflammation proteins, which in turn leads to insulin production. Obese individuals have higher moribund adipocytes and thus more macrophages. The presence of these inflammation proteins results in large insulin resistivity and perpetuate obesity. This seems like an awful endless cycle. Now I know how I get fat so easily. This sucks!

Sequelae of obesity: That pretty much sums up my life.

The good thing adiponectin is an inhibitor of those inflammation proteins, but unfortunately that production decreases as you get fatter. It seems there are two main proinflammatory proteins, TNF-α and IL-6. TNF-α sucks balls, but IL-6 sucks more balls. TNF-α breaks down fatty cells in a process called lipolysis. That sounds good except that too much of this (from really fat cells) floods neighboring tissue (through free fatty acids) and promotes insulin resistance. IL-6 on the other hand does the exact same thing as TNF-α (by inducing lipolysis and making you fat), but it is nearly 10 times more prominent in the body than TNF-α in obese individuals. That sucks!

Oh yea, there is cortisol to worry about too, but I won't scare you or myself too much today.

What I Learned

I want to eat. My leptin (which I apparently don't have) tells me to eat a little. If I eat a lot, my body produces things that prevent the proper metabolism of the food I ingest and makes me even fatter than when I just ate a lot. Great. Fuck life!