Not done by insulin:

Ketogenesis Repeat,from May 09 Lack of insulin promotes ketogenesis. Insulin prevents ketngenesis. Metabolic Effects of Insulin Insulin is known as hormone of abundance. When there is great abundance of energy-giving foods in the diet, especially excess amounts of carbohydrates, insulin is secreted in large amounts. The net effect of insulin is storage of carbohydrate, protein, and fat. Therefore, insulin is called the hormone of abundance. In the case of excess carbohydrates, it causes them to be stored as glycogen mainly in the liver and muscles. Also, all the excess carbohydrates that cannot be stored as glycogen are conveed under the stimulus of insulin into fats and stored in the adipose tissue. In the case of proteins, insulin has a direct effect in promoting amino acid uptake by cells and conversion of these amino acids into protein. In addition, it inhibits the breakdown of the proteins that are already in the cells. Effect of Insulin on Carbohydrate Metabolism Immediately after a high-carbohydrate meal, the glucose that is absorbed into the blood causes rapid secretion of insulin. The insulin in turn causes rapid uptake, storage, and use of glucose by almost all tissues of the body, but especially by the muscles, adipose tissue, and liver. Insulin promotes liver uptake and storage as glycogen One of the most impoant of all the effects of insulin is to cause most of the glucose absorbed after a meal to be stored almost immediately in the liver in the form of glycogen. Then, between meals, when food is not available and the blood glucose concentration begins to fall, insulin secretion decreases rapidly and the liver glycogen is split back into glucose, which is released back into the blood to keep the glucose concentration from falling too low. The mechanism by which insulin causes glucose uptake and storage in the liver includes several almost simultaneous steps: Insulin inactivates liver phosphorylase, the principal enzyme that causes liver glycogen to split into glucose. This prevents breakdown of the glycogen that has been stored in the liver cells. Insulin increases the activity of the enzyme glucokinase, which is one of the enzymes that causes the initial phosphorylation of glucose after it diffuses into the liver cells. Once phosphorylated, the glucose is temporarily trapped inside the liver cells because phosphorylated glucose cannot diffuse back through the cell membrane. iii. Insulin also increases the activities of the enzymes that promote glycogen synthesis, including especially glycogen synthase, which is responsible for polymerization of the monosaccharide units to form the glycogen molecules. Insulin Promotes Conversion of Excess Glucose into Fatty Acids When the quantity of glucose entering the liver cells is more than can be stored as glycogen or can be used for local hepatocyte metabolism, insulin promotes the conversion of all this excess glucose into fatty acids. These fatty acids are subsequently packaged as triglycerides in very-low-density lipoproteins and transpoed in this form by way of the blood to the adipose tissue and deposited as fat. Insulin also inhibits gluconeogenesis. Insulin Promotes Muscle Glucose Uptake and Metabolism Without insulin muscle membrane is only slightly permeable to glucose. Thus between meals, non-exercising muscles, derive their energy from fatty acids, not on glucose. In the presence of insulin, muscle membrane become permeable to glucose. If the muscles are not exercising after a meal and yet glucose is transpoed into the muscle cells in abundance, then most of the glucose is stored in the form of muscle glycogen instead of being used for energy. The glycogen can later be used for energy by the muscle. Effect of Insulin on Carbohydrate Metabolism in Other Cells Insulin increases glucose transpo into and glucose usage by most other cells of the body (with the exception of the brain cells, as noted) in the same way that it affects glucose transpo and usage in muscle cells. Effect of Insulin on Fat Metabolism Although not quite as visible as the acute effects of insulin on carbohydrate metabolism, insulin's effects on fat metabolism are, in the long run, equally impoant. Long-term effect of insulin lack causes extreme atherosclerosis, often leading to hea attacks, cerebral strokes, and other vascular accidents. Insulin Promotes Fat Synthesis and Storage Fat sparing effect-Insulin has several effects that lead to fat storage in adipose tissue. First, insulin increases the utilization of glucose by most of the body's tissues, which automatically decreases the utilization of fat, thus functioning as a fat sparer. Insulin also promotes fatty acid synthesis. Synthesis of fat in liver-When more carbohydrates are ingested than can be used for immediate energy, are used for fat synthesis. Almost all this synthesis occurs in the liver cells, and the fatty acids are then transpoed from the liver by way of the blood lipoproteins to the adipose cells to be stored. Storage of fat in the adipose Cells. Insulin has two other essential effects that are required for fat storage in adipose cells: Insulin inhibits the action of hormone-sensitive lipase. This is the enzyme that causes hydrolysis of the triglycerides already stored in the fat cells. Therefore, the release of fatty acids from the adipose tissue into the circulating blood is inhibited. Insulin promotes glucose transpo through the cell membrane into the fat cells in exactly the same ways that it promotes glucose transpo into muscle cells. Some of this glucose is then used to synthesize minute amounts of fatty acids, but more impoant, it also forms large quantities of a-glycerol phosphate. This substance supplies the glycerol that combines with fatty acids to form the triglycerides that are the storage form of fat in adipose cells. Therefore, when insulin is not available, even storage of the large amounts of fatty acids transpoed from the liver in the lipoproteins is almost blocked. Insulin Deficiency Increases Use of Fat for Energy Insulin Deficiency Causes Lipolysis of Storage Fat and Release of Free Fatty Acids. In the absence of insulin, hormone-sensitive lipase in the fat cells becomes strongly activated. This causes hydrolysis of the stored triglycerides, releasing large quantities of fatty acids and glycerol into the circulating blood. This free fatty acid then becomes the main energy substrate used by essentially all tissues of the body besides the brain. Insulin Deficiency Increases Plasma Cholesterol and Phospholipid Concentrations. The excess of fatty acids in the plasma associated with insulin deficiency also promotes liver conversion of some of the fatty acids into phospholipids and cholesterol, two of the major products of fat metabolism. This high lipid concentration--especially the high concentration of cholesterol--promotes the development of atherosclerosis in people with serious diabetes. Excess Usage of Fats During Insulin Lack Causes Ketosis and Acidosis. Insulin lack also causes excessive amounts of acetoacetic acid to be formed in the liver cells. Some of the acetoacetic acid is also conveed into 13-hydroxybutyric acid and acetone. These two substances, along with the acetoacetic acid, are called ketone bodies, and their presence in large quantities in the body fluids is called ketosis. In severe diabetes the acetoacetic acid and the I3-hydroxybutyric acid can cause severe acidosis and coma, which often leads to death. Effect of Insulin on Protein Metabolism Insulin Promotes Protein Synthesis and Storage. During the few hours after a meal when excess quantities of nutrients are available in the circulating blood, not only carbohydrates and fats but proteins as well are stored in the tissues; insulin is required for this to occur. The manner in which insulin causes protein storage is not as well understood as the mechanisms for both glucose and fat storage. Some of the facts follow. Insulin stimulates transpo of many of the amino acids into the cells. Among the amino acids most strongly transpoed are valine, leucine, isoleucine, tyrosine, and phenylalanine. Insulin increases the translation of messenger RNA, thus forming new proteins. Over a longer period of time, insulin also increases the rate of transcription of selected DNA genetic sequences in the cell nuclei, thus forming increased quantities of RNA and still more protein synthesis--especially promoting a vast array of enzymes for storage of carbohydrates, fats, and proteins. 4. Insulin inhibits the catabolism of proteins, thus decreasing the rate of amino acid release from the cells, especially from the muscle cells. 5. In the liver, insulin depresses the rate of gluconeogenesis. Because the substrates most used for synthesis of glucose by gluconeogenesis are the plasma amino acids, this suppression of gluconeogenesis conserves the amino acids in the protein stores of the body. In summary, insulin promotes protein formation and prevents the degradation of proteins. Note that: The brain is quite different from most other tissues of the body in that insulin has little effect on uptake or use of glucose. Instead, the brain cells are permeable to glucose and can use glucose without the intermediation of insulin. The brain cells are also quite different from most other cells of the body in that they normally use only glucose for energy and can use other energy substrates, such as fats, only with difficulty.Therefore, it is essential that the blood glucose level always be maintained above a critical level, which is one of the most impoant functions of the blood glucose control system. When the blood glucose falls too low, into the range of 20 to 50 mg/100 ml. symptoms of hypoglycemic shock develop, characterized by progressive nervous irritability that leads to fainting, seizures, and even coma. Summary: Effects of Insulin on various tissues: Liver Increased glycogen synthesis Increased protein synthesis Increased lipid synthesis Decreased ketogenesis Decreased glucose output due to decreased gluconeogenesis, increased glycogen synthesis, and increased glycolysis. Muscle Increased glucose entry Increased glycogen synthesis Increased amino acid uptake Increased protein synthesis Decreased protein catabolism Decreased release of gluconeogenic amino acids Increased ketone uptake Increased K+ uptake Adipose tissue Increased glucose entry Increased. fatty acid synthesis Increased glycerol phosphate synthesis Increased triglyceride deposition Activation of lipoprotein lipase Inhibition of hormone -sensitive lipase Increased K+ uptake