Beta cell
[3] The function of beta cells is primarily centered around the synthesis and secretion of hormones, particularly insulin and amylin.
[5] Amylin helps regulate the rate at which glucose enters the bloodstream after a meal, slowing down the absorption of nutrients by inhibit gastric emptying.
[7] As glucose stimulates insulin secretion, it simultaneously increases proinsulin biosynthesis through translational control and enhanced gene transcription.
[4] After translation, the preproinsulin precursor contains an N-terminal signal peptide that allows translocation into the rough endoplasmic reticulum (RER).
[9] After maturation, these secretory vesicles hold insulin, C-peptide, and amylin until calcium triggers exocytosis of the granule contents.
[15] Since beta cells use glucokinase to catalyze the first step of glycolysis, metabolism only occurs around physiological blood glucose levels and above.
[17] As a result, the potential difference across the membrane becomes more positive (as potassium ions accumulate inside the cell).
[11] Beta cells have significant clinical relevance as their proper function is essential for glucose regulation, and dysfunction is a key factor in the development and progression of diabetes and its associated complications.
[27] The symptoms of diabetes can potentially be controlled with methods such as regular doses of insulin and sustaining a proper diet.
[4] It is believed to be due to the decline of specific receptors on the surface of the liver, adipose, and muscle cells which lose their ability to respond to insulin that circulates in the blood.
[4] However, the beta cells can become overworked and exhausted from being overstimulated, leading to a 50% reduction in function along with a 40% decrease in beta-cell volume.
[9] At this point, not enough insulin can be produced and secreted to keep blood glucose levels within their normal range, causing overt type 2 diabetes.
Insulinomas are usually benign, but may be medically significant and even life-threatening due to recurrent and prolonged attacks of hypoglycemia.
Diabetes mellitus can be experimentally induced in vivo for research purposes by streptozotocin[34] or alloxan,[35] which are specifically toxic to beta cells.
[37] While these studies have conclusive results in mice, beta cells in human subjects may not possess this same level of versatility.
An unlimited amount of beta cells produced artificially could potentially provide therapy to many of the patients who are affected by Type 1 diabetes.
