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This animation describe the role of insulin and the pancreas in diabetes.

Impaired insulin function can lead to a condition called diabetes mellitus    , the main symptoms of which are illustrated in [link] . This can be caused by low levels of insulin production by the beta cells of the pancreas, or by reduced sensitivity of tissue cells to insulin. This prevents glucose from being absorbed by cells, causing high levels of blood glucose, or hyperglycemia    (high sugar). High blood glucose levels make it difficult for the kidneys to recover all the glucose from nascent urine, resulting in glucose being lost in urine. High glucose levels also result in less water being reabsorbed by the kidneys, causing high amounts of urine to be produced; this may result in dehydration. Over time, high blood glucose levels can cause nerve damage to the eyes and peripheral body tissues, as well as damage to the kidneys and cardiovascular system. Oversecretion of insulin can cause hypoglycemia    , low blood glucose levels. This causes insufficient glucose availability to cells, often leading to muscle weakness, and can sometimes cause unconsciousness or death if left untreated.

Symptoms of diabetes include excessive thirst, excessive hunger, lethargy and stupor, blurred vision, weight loss, breath that smells like acetone, hyperventilation, nausea, vomiting, abdominal pain, frequent urination, and glucose in the urine.
The main symptoms of diabetes are shown. (credit: modification of work by Mikael Häggström)

When blood glucose levels decline below normal levels, for example between meals or when glucose is utilized rapidly during exercise, the hormone glucagon    is released from the alpha cells of the pancreas. Glucagon raises blood glucose levels, eliciting what is called a hyperglycemic effect, by stimulating the breakdown of glycogen to glucose in skeletal muscle cells and liver cells in a process called glycogenolysis    . Glucose can then be utilized as energy by muscle cells and released into circulation by the liver cells. Glucagon also stimulates absorption of amino acids from the blood by the liver, which then converts them to glucose. This process of glucose synthesis is called gluconeogenesis    . Glucagon also stimulates adipose cells to release fatty acids into the blood. These actions mediated by glucagon result in an increase in blood glucose levels to normal homeostatic levels. Rising blood glucose levels inhibit further glucagon release by the pancreas via a negative feedback mechanism. In this way, insulin and glucagon work together to maintain homeostatic glucose levels, as shown in [link] .

Art connection

When blood glucose levels fall, the pancreas secretes the hormone glucagon. Glucagon causes the liver to break down glycogen, releasing glucose into the blood. As a result, blood glucose levels rise. In response to high glucose levels, the pancreas releases insulin. In response to insulin, target cells take up glucose, and the liver converts glucose to glycogen. As a result, blood glucose levels fall.
Insulin and glucagon regulate blood glucose levels.

Pancreatic tumors may cause excess secretion of glucagon. Type I diabetes results from the failure of the pancreas to produce insulin. Which of the following statement about these two conditions is true?

  1. A pancreatic tumor and type I diabetes will have the opposite effects on blood sugar levels.
  2. A pancreatic tumor and type I diabetes will both cause hyperglycemia.
  3. A pancreatic tumor and type I diabetes will both cause hypoglycemia.
  4. Both pancreatic tumors and type I diabetes result in the inability of cells to take up glucose.

Hormonal regulation of stress

When a threat or danger is perceived, the body responds by releasing hormones that will ready it for the “fight-or-flight” response. The effects of this response are familiar to anyone who has been in a stressful situation: increased heart rate, dry mouth, and hair standing up.

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Source:  OpenStax, Bmcc 103 - concepts of biology. OpenStax CNX. Aug 06, 2015 Download for free at https://legacy.cnx.org/content/col11855/1.2
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