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- J Endocrinol. 2002 Aug;174(2):225-31.
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Mechanisms involved in the beta-cell mass increase induced by chronic sucrose feeding to normal rats.
CENEXA, Centre of Experimental and Applied Endocrinology (UNLP-CONICET), University of La Plata School of Medicine, La Plata, Argentina.
- The aim of the present study was to clarify the mechanisms by which a sucrose-rich diet (SRD) produces an
increase in the pancreatic beta-cell mass in the rat.
- Normal Wistar rats were fed for 30 weeks either an SRD (SRD rats; 63% wt/wt), or the same diet but with starch instead of sucrose in the same proportion (CD rats).
- We studied body weight, serum glucose and triacylglycerol levels, endocrine tissue and beta-cell mass, beta-cell replication rate (proliferating cell nuclear antigen; PCNA), islet neogenesis (cytokeratin immunostaining) and beta-cell apoptosis (propidium iodide).
- Body weight (g) recorded in the SRD rats was significantly (P<0.05)
- Both serum glucose and triacylglycerol levels (mmol/l) were also significantly higher (P<0.05)
The number of pancreatic islets per unit area increased significantly (P<0.05)>
- A significant increment (2.6 times) in the mass of endocrine tissue was detected in SRD animals, mainly due to an increase in the beta-cell mass (P=0.0025).
- The islet cell replication rate, measured as the percentage of PCNA-labelled beta cells increased 6.8 times in SRD rats (P<0.03).
- The number of apoptotic cells in the endocrine pancreas decreased significantly (three times) in the SRD animals (P=0.03).
- The cytokeratin-positive area did not show significant differences between CD and SRD rats.
The increase of beta-cell mass induced by SRD was accomplished by an enhanced replication of beta cells together with a decrease in the rate of beta-cell apoptosis, without any evident participation of islet neogenesis.
- This pancreatic reaction was unable to maintain serum glucose levels of these rats at the level measured in CD animals.
- A significant increment (2.6 times) in the mass of endocrine tissue was detected in SRD animals, mainly due to an increase in the beta-cell mass (P=0.0025).
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Related Articles
- Islet neogenesis: an apparent key component of long-term pancreas adaptation to increased insulin demand. [J Endocrinol. 2004]
- Changes induced by sucrose administration upon the morphology and function of pancreatic islets in the normal hamster. [Diabetes Metab Res Rev. 1999]
- Possible relationship between changes in islet neogenesis and islet neogenesis-associated protein-positive cell mass induced by sucrose administration to normal hamsters. [J Endocrinol. 2000]
- A low protein diet alters the balance of islet cell replication and apoptosis in the fetal and neonatal rat and is associated with a reduced pancreatic expression of insulin-like growth factor-II. [Endocrinology. 1999]
- Multiphasic metabolic changes in the heart of rats fed a sucrose-rich diet. [Horm Metab Res. 1994]
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- Patient Drug Information
- Glucagon (GlucaGen Diagnostic Kit®) Glucagon is a hormone produced in the pancreas. Glucagon is used to raise very low blood sugar. Glucagon is also used in diagnostic testing of the stomach and other digestive organs.
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http://joe.endocrinology-journals.org/cgi/content/abstract/174/2/225
Beta cells (beta-cells, β-cells) are a type of cell in the pancreas in areas called the islets of Langerhans. They make up 65-80% of the cells in the islets.
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Function
Beta cells make and release insulin, a hormone that controls the level of glucose in the blood. There is a baseline level of insulin maintained by the pancreas, but it can respond quickly to spikes in blood glucose by releasing stored insulin while simultaneously producing more. The response time is fairly quick, taking approximately 10 minutes.
Apart from insulin, beta cells release C-peptide, a byproduct of insulin production, into the bloodstream in equimolar quantities. C-peptide helps to prevent neuropathy, and other symptoms of diabetes related to vascular deterioration[1]. Measuring the levels of C-peptide can give a practitioner an idea of the viable beta cell mass.[2]
β-cells also produce amylin,[3] 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. It thus functions as a synergistic partner to insulin. Whereas insulin regulates long term food intake, increased amylin decreases food intake in the short term.
Pathology
- Diabetes mellitus type 1 is caused by the destruction or dysfunction of insulin-producing beta cells by the cells of the immune system.
- In Diabetes mellitus type 2, by contrast, beta cells decline gradually over time, and insulin resistance plays at least as large a role in the disease [4][5]
- Insulinoma is a rare tumor (usually benign) derived from beta cells. It results in recurrent and prolonged attacks of hypoglycemia.
Research
Much research is being done in the field of beta-cell physiology and pathology. One major research topic is its effects on diabetes. Many researchers are trying to find ways to use these beta-cells to help control or prevent diabetes. A major topic is the replication of adult beta-cells and the application of these to diabetes. The Larry L. Hillblom Islet Research Center at UCLA[6] is a leading research center in the field, within the Diabetes and Endocrinology Research Center[7], directed by Dr. Peter Butler. [8]
A team science effort also exists, known as the Beta Cell Biology Consortium (BCBC).[9] The BCBC is responsible for facilitating interdisciplinary approaches that will advance the understanding of pancreatic islet development and function. The long-term goal of the BCBC is to develop a cell-based therapy for insulin delivery.
In a study presented on June 8, 2008 at the American Diabetes Association’s 68th Scientific Sessions, a team showed that mice lacking insulin receptors in their beta cells had problems in the processing of insulin leading to excess, unprocessed levels of the hormone. Unprocessed insulin is unable to properly control glucose levels in the body. High circulating levels of unprocessed insulin and insulin resistance, a condition in which normal amounts of insulin are inadequate to produce a normal insulin response, are both known to be early indicators of type 2 diabetes.[10]
See also
References
- ^ Y. Ido, A. Vindigni, K. Chang, L. Stramm, R. Chance, W. F. Heath, R. D. DiMarchi, E. Di Cera, J. R. Williamson. 1997. Prevention of Vascular and Neural Dysfunction in Diabetic Rats by C-Peptide. Science, Vol. 277. no. 5325, pp. 563 - 566.
- ^ Hoogwerf B, Goetz F (1983). "Urinary C-peptide: a simple measure of integrated insulin production with emphasis on the effects of body size, diet, and corticosteroids". J Clin Endocrinol Metab 56 (1): 60–7. PMID 6336620.
- ^ Moore C, Cooper G (1991). "Co-secretion of amylin and insulin from cultured islet beta-cells: modulation by nutrient secretagogues, islet hormones and hypoglycemic agents". Biochem Biophys Res Commun 179 (1): 1–9. doi:. PMID 1679326.
- ^ "U.K. prospective diabetes study 16. Overview of 6 years' therapy of type II diabetes: a progressive disease. U.K. Prospective Diabetes Study Group" (1995). Diabetes 44 (11): 1249–58. doi:. PMID 7589820.
- ^ Rudenski A, Matthews D, Levy J, Turner R (1991). "Understanding "insulin resistance": both glucose resistance and insulin resistance are required to model human diabetes". Metabolism 40 (9): 908–17. doi:. PMID 1895955.
- ^ The Larry L. Hillblom Islet Research Center
- ^ The DERC Homepage has moved
- ^ Faculty
- ^ Beta Cell Biology Consortium
- ^ Newswise: Beta Cell Defect Linked to Type 2 Diabetes Retrieved on June 8, 2008.
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