Type 2 diabetes is the type of diabetes that occurs later in life. Insulin resistance precedes the development of type 2 diabetes, sometimes by years. In individuals who will ultimately develop type 2 diabetes, it is believed that blood glucose and insulin levels are normal for many years; then at some point in time, insulin resistance develops.
At this point, there is often an association of high insulin levels, central obesity, cholesterol abnormalities, and /or high blood pressure (hypertension). When this constellation of disease processes occur, it is know as the metabolic syndrome.
One of the actions of insulin is to cause the cells of the body, particularly the muscle and fat cells, to remove and use glucose from the blood. This is one way in which insulin controls the level of glucose in blood. Insulin has this effect on the cells by binding to insulin receptors on the surface of the cells. You can think of it as insulin "knocking" on the doors of muscle and fat cells. The cells hear the knock, open up, and let glucose in to be used by the cell. With insulin resistance, the muscles don't hear the knock as well (they are resistant), and the pancreas is notified that it needs to make more insulin, which increases the level of insulin in the blood and causes a louder knock.
The resistance of the cells continues to increase over time. As long as the pancreas is able to produce enough insulin to overcome this resistance, blood glucose levels remain normal. When the pancreas can no longer produce enough insulin, the blood glucose levels begin to rise, initially after meals when glucose levels are at their highest and more insulin is needed, but eventually in the fasting state too. At this point, type 2 diabetes is present.
With the decrease in air quality, asthma has become a very prevalent condition, especially in Western societies. An asthma allergy is often seen in children and adolescents, with it being less common in adults. Even though it is less common in adults, it is still possible for many adults to be diagnosed and suffer from asthma.
An asthma allergy is a condition in which targets the respiratory system. An irritant is breathed into the lungs, and this goes on to cause inflammation of the tubes of the lungs called the bronchi and bronchioles. This inflammation initiates release of chemicals that causes the entrances to the lung tissue to constrict. The result of this is the coughing sound produced along with any wheezing.
Even though there has not been a gene located that shows if someone will be diagnosed with asthma or not, asthma allergy does have a tendency to run in families. Therefore, scientist believe that if you have a parent with asthma, and depending on you genetic makeup, you run the risk of being predisposed to a diagnosis of asthma. Your risk of been diagnosed with an asthma allergy increases if you also have a sibling who has also been diagnosed with asthma.
However, even though asthma allergy might have a genetic tendency, the environment still plays a factor in the flare up of an attack. For example, being around pets, cigarette smoke, and dust mites can lead to an asthma attack for some people. Anyone with should try to avoid conditions that might triggers there asthma.
It seems that some people are destined to be skinny. They have never known being fat, and they make being thin look easy. Others of us are in the opposite situation. It is a struggle to lose weight, and being thin seems impossible. Could it be that our genes have something to do with it? As it turns out, there are several genes that play a role in obesity. Defects in some of these genes cause certain syndromes to develop. Not everything is known about the genetics of obesity, but our knowledge is expanding.
A part of the brain called the hypothalamus controls several functions of the body. One of these is the regulation of the sense of hunger. There is an interplay between various chemical messengers and the hypothalamus. This interplay is called the hypothalamic leptin-melanocortin system. Our fat cells make a signal called leptin. The more fat we have, the more leptin is produced. It binds to the leptin receptor in the hypothalamus. The hypothalamus senses a minimal amount of leptin which tells the brain that the body has at least the required amount of fat to function. Once the receptor is activated, a protein called proopiomelanocortin (POMC) is made. POMC is then cut into smaller parts by enzymes. One of these enzymes is proenzyme convertase 1 (PC-1). One of the smaller proteins produced by PC-1 is called alpha-MSH which binds another receptor in the hypothalamus called MC4R. Once MC4R is turned on, it triggers some intracellular signals that end up telling your brain that you are not as hungry. Got all that?! Check out the link at the end of this article and go to the "Genetics" tab. On the "leptin" page, there is a diagram that explains it.
A defect in the genes for any of the signals, enzymes, and receptors mentioned above can lead to an increased appetite. The most common of these mutations is a defect in MC4R. However, it is not the most severe, and some people with a defective MC4R gene are still thin. Mutations in other genes cause a voracious appetite in very young children, and they are nearly destined to eat far more than their bodies will ever need. In addition to becoming very obese, associated problems can include: small ovaries and testicles, thyroid dysfunction, decreased immunity, and low functioning adrenal glands. Fortunately, these more severe conditions are rare with only a handful of known cases. There are treatments for a few, like replacing leptin with shots. For others, like MC4R, there are to treatments.
A few genes that aid in the development of the hypothalamus are also associated with obesity. The SIM1 gene encodes signals that come from the MC4R receptor. One case of a young girl with a SIM1 mutation was obese and also tall. In addition to development of the hypothalamus, the tropomysin-related kinase B (TrkB) receptor and the chemical signal called brain-derived neutrotrophic factor (BDNF) play roles in memory, behavior, and intellect. Defects in either of these two can cause obesity and memory problems.
In the reward center of the brain, dopamine is released when we eat food. People who have mutations in a stretch of DNA called TaqIA have fewer dopamine receptors and thus need to eat more to feel the same sense of reward. This lends weight to the fact that some people may literally be addicted to food, and the sweeter the food, the stronger the addiction.
There are also several genetic syndromes associated with obesity that involve more than one gene. They are too complex for this article, but here is a list of some of them: Prader-Willi, Bardet-Biedl, Ahlstrom, Cohen, and Carpenter syndromes.
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