As periodic eaters, humans need insulin to survive. Insulin helps the body store energy to fuel the body’s continuous needs and activities. Insulin is secreted after eating in order to store energy (e.g. glucose, amino acids) into the liver, muscle and adipose tissue (fat)—the body’s primary fuel source. Within about an hour after a meal, insulin levels diminish, leading to an increase in the hormone glucagon. Glucagon signals the body to begin releasing stored energy (glycogen from the liver and muscle, and fatty acids from adipose tissue) into the blood stream to fuel the body’s continuous energy needs, essentially reversing the actions of insulin. This cycle is repeated with every meal.
Insulin plays a major role in keeping us alive, but in short, this hormone is not responsible for weight loss or continuous body fat gains. Only we are in control of our weight. Whether one increases or decreases the size of their fat stores from day to day depends upon the relationship of calories eaten to the amount of calories used through metabolism and daily activity. If, at the end of the day, you are in a caloric deficit (more calories/fat burned than stored), then fat stores will decrease. However, if calories eaten exceed calories used, body fat stores will increase.[2,3] Insulin is just doing its job, which is storing things, including amino acids, to build muscle. However, it is the person, through eating, who gives insulin the "things" to store. In other words, insulin does not cause a person to become fat. The excess food one consumes leads to the average adult’s growing waistline, and of course that is 100% under the control of the person eating the calories.
1 Hunt SM; Groff JL. 1995. Advanced Nutrition and Human Metabolism. St. Paul, MN: West Publishing Company. 578pgs.
2 Tipton KD, Witard OC. Protein requirements and recommendations for athletes: relevance of ivory tower arguments for practical recommendations. Clin Sports Med. 2007 Jan;26(1):17-36. Review.
3 Sun SZ, EmpieMW. Lack of findings for the association between obesity risk and the usual sugar-sweetened beverage consumtion in adults- A primary analysis of databases of CSFII-1989-1991, CSFII-1994-1998, NHANES III and combined NHANES 1999-2002. Food Chem Toxicol. 2007. 45 (8): 1523-1536.