**2. Beta cells functions**

Insulin is synthesized as preproinsulin in the ribosomes of the rough endoplasmic reticulum in the beta cells (fig 1). Preproinsulin is then cleaved to proinsulin, which is transported to the Golgi apparatus where it is packaged into secretory granules located close to the cell membrane. Proinsulin is cleaved into equimolar amounts of insulin and C-peptide in the se‐ cretory granules. The process of insulin secretion involves fusion of the secretory granules with the cell membrane and exocytosis of insulin, C-peptide, and proinsulin

© 2013 Nepton; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Insulin is a hormone that controls the blood glucose concentration. The liver maintains the base-line glucose level, but the beta cells can respond quickly to spikes in blood glucose by releasing some of its stored insulin while simultaneously producing more. The response time is very quick.

contain their own special zinc transporter called zinc transporter 8 that enables beta cells to take up zinc.Gene alterations in this zinc transporter are now known to cause type II diabetes while type I diabetes is associated with antibodies against this zinc transporter (meaning the

Beta-Cell Function and Failure http://dx.doi.org/10.5772/52153 117

Zinc directly influences how insulin is produced and secreted by our beta cells. So the peo‐ ple with zinc deficiency can't store and release insulin.Furthermore, zinc is self-protecting to the beta cells.It has now been shown that zinc directly reduces the inflammatory signals that

The secretion of insulin from pancreatic beta cells is a complex process involving the inte‐ gration and interaction of multiple external and internal stimuli. Thus, nutrients, hormones, neurotransmitters, and drugs all activate or inhibit insulin secretion. The primary stimulus for insulin release is the beta-cell response to changes in glucose concentration. Normally, glucose induces a biphasic pattern of insulin release. First-phase insulin release occurs with‐ in the first few minutes after exposure to an elevated glucose level; this is followed by a more permanent second phase of insulin release. Of particular importance is the observation that first-phase insulin secretion is lost in patients with type 2 diabetes. Thus, molecular mechanisms involved in phasic insulin secretion are important. This processes discussed as

A widely accepted sequence of events involved in glucose-induced insulin secretion is as

immune system knocks out function of beta cells so they can't produce insulin).

damage the beta cells, a process that leads to type I diabetes.

**3. Mechanisms of insulin secretion from beta cells**

follow (fig 2).

**Figure 2.** The beta cell structure

follows:

**Figure 1** Mouse pancreatic islet as seen by light microscopy. Beta cells can be recognized by the green insulin staining. Glucagon is labeled in red and the nuclei in blue

Apart from insulin, beta cells release C-peptide, a consequence of insulin production, into the bloodstream in equimolar amounts. C-peptide helps to prevent neuropathy and other symptoms of diabetes related to vascular deterioration.Measuring the levels of C-peptide can give a practitioner an idea of the viable beta cell mass.

Beta-cells also produce amylin, also known as IAPP, islet amyloid polypeptide. Amylin functions as part of the endocrine pancreas and contributes to glycemic control. Amylin's metabolic function is now somewhat well characterized as an inhibitor of the appearance of nutrient [especially glucose] in the plasma. Thus, it functions as a synergistic partner to in‐ sulin. Whereas insulin regulates long-term food intake, increased amylin decreases food in‐ take in the short term.

GABA (γ amino butyric acid) is produced by pancreatic beta cell. GABA released from beta cells can act on GABA Areceptor in the α cells, causing membrane hyperpolarization and hence suppressing glucagon secretion. An impaired insulin-Akt-GABAA receptors glucagon secretory pathway in the islet may be an underlying mechanism for unsuppressed glucagon secretion, despite hyperglycemia, in diabetic subjects. Some studies demonstrated that beta cells also express GABA A receptors, forming an autocrine GABA signaling system. Howev‐ er, the role of this autocrine GABA signaling in the regulation of beta cell functions remains largely unknown.

Zinc is needed by over 300 enzyme systems.Some of those are involved with the metabolism of blood sugar and are so important that a lack of zinc, in and of itself, can cause type I or type II diabetes.

Zinc is highly concentrated in the insulin-secreting beta cells of our pancreas. Zinc can keep in‐ sulin molecules together in the beta cells.Beta cells must have zinc to function. In fact, beta cells contain their own special zinc transporter called zinc transporter 8 that enables beta cells to take up zinc.Gene alterations in this zinc transporter are now known to cause type II diabetes while type I diabetes is associated with antibodies against this zinc transporter (meaning the immune system knocks out function of beta cells so they can't produce insulin).

Zinc directly influences how insulin is produced and secreted by our beta cells. So the peo‐ ple with zinc deficiency can't store and release insulin.Furthermore, zinc is self-protecting to the beta cells.It has now been shown that zinc directly reduces the inflammatory signals that damage the beta cells, a process that leads to type I diabetes.
