In a healthy person

Normally, the pancreas makes enough insulin to keep the supply and use of glucose in balance. When the blood contains enough insulin, the liver temporarily shuts down its production of glucose, and glucose is transported from the blood into your cells. Cells use some of the glucose immediately. Most of the remainder is converted to a substance called glycogen in the liver and muscles, where it is stored for future use. The body's ability to store glycogen is limited, and any excess glucose that does not get stored as glycogen is converted to triglycerides and stored in adipose (fat) tissue.

Pancreatic cells in the islets of Langerhans continuously monitor blood glucose levels. After a meal, the carbohydrates you eat are digested and broken down into glucose and other sugars, which pass into the bloodstream. As your blood glucose levels rise, beta cells in the pancreas respond by secreting insulin into the blood. Glucose then passes into your cells and the liver shuts down glucose production. Between meals, insulin also prevents excessive release of glucose from the liver into the bloodstream. If blood glucose levels drop too low between meals, alpha cells in the pancreas release a hormone called glucagon. This hormone signals the liver to convert amino acids and glycogen into glucose that is sent into the blood.

In a person with diabetes

In diabetes, this glucose balancing system is disrupted, either because too little insulin is produced or because the body's cells do not respond to insulin normally (a condition called insulin resistance). The result is an unhealthy rise in blood glucose levels. If diabetes is left untreated, the two principal dangers are the immediate results of high blood glucose levels (which include excessive urination, dehydration, intense thirst, and fatigue) and long-term complications that can affect your eyes, nerves, kidneys, and large blood vessels.

Publication Review By: Written by: Christopher D. Saudek, M.D.; Simeon Margolis, M.D., Ph.D.

Published: 19 Apr 2009

Last Modified: 11 Sep 2015