We know as dietitians or well, just regular people that obesity is caused by too much (food) and not enough (activity). This post will focus on the appetite center and hormones. For the sake of sanity and brevity this will provide brief insight about the function of appetite and how weight loss surgery relates to these functions.
What really causes us to eat? Appetite control comes from the hypothalamus, arcuate neurons located here control hormone and lipid levels, along with metabolites which affect metabolism and hunger.
"The hypothalamus controls appetite and coordinates this with energy utilization. It is, therefore, responsible for maintenance of body weight, carefully adjusting food intake to physical activity. Loss of sensitivity to hormones and metabolites in the arcuate nucleus can lead to unbalanced energy intake and use, resulting in overweight and obesity." (1)
The arcuate nucleus has two different neurons: primary neurons that stimulate appetite with neuropeptide Y and agouti-related peptide; the arcuate also has neurons called proopiomelanocortin that depress appetite. So therefore the body has a sense of checks and balances to a point.
Some additional factors that contribute to appetite are hormones. They are insulin, leptin, ghrelin, and a crazy gut hormone called PYY 3-36.
We know about insulin with the diabetes epidemic, this hormone from the pancreas shuttles glucose (blood sugar, i.e. energy) into the cells so they can do their thing (reproduce, work, whatever).
Grehlin and PYY both come from the stomach and digestive track. Ghrelin stimulates neuropeptide Y and agouti-related peptide (mentioned above). PYY comes from endocrine cells located in the intestines. It basically shuts off Grehlin and it's pro-eating peptide buddies. The only drawback is that it takes 20 minutes to work and some of us know how much we can shovel in during that period.
Additional hormones that come from the digestive track that regulate appetite/weight functions are also: Cholecystokinin (CCK), Glucose-dependent Insulinotrophic Peptide and Glugagon-Like Peptide (GLP-1).
CCK comes from the intestine and is triggered by protein and fat. It decreases gastric emptying (you feel full longer) and slows hunger. It acts when food enters the duodenum of the intestine.
Glucose-dependent Insulinotrophic Peptide also comes from the intestine besides being a long word. It is released when glucose (carbohydrates) and free fatty acids come through. It helps the body move energy-rich foods or Twinkees into storage, i.e. fat. This is a good example of our caveman (and cave-woman) ancestors tracking down a mastodon and converting Calories into energy and for storage. Since you might not know when the next woolly mammoth will come down your street.
Glugagon-Like Peptide (GLP-1) also causes a 'full' sensation by preventing calorie loss in the stool and comes from the illeum (again another function from our caveman ancestors). It also stimulates insulin and it believed to act as a key player in diabetics who have gastric bypass done. This is when health professionals may say that it "cures" Type II Diabetes. On the other hand, it can also cause hypogylcemia in these individuals where their blood sugar drops out of the normal range.
"Obesity and metabolic surgeries initially were thought to restore balance to the system primarily by minimizing intake of excess calories through restriction or malabsorption. However, while these operations can limit the quantity of food consumed, they each bring on a different change in GI hormone profiles following surgery. As more enterohormonal mechanisms are discovered and understood, operations or drug therapies may be tailored to maximize the treatment of obesity and diabetes, achieving optimal results with minimal metabolic complications." (2)
1. "Appetite and Metabolism and Obesity."
2. Daniel J. Rosen, MD; and Alfons Pomp, MD, FACS, . "Gastrointestinal Hormones and their Relationship to Bariatric Surgery." . Bariatric Times, 04/2009. Web. 20 May 2012.