Role of Beta-Glucan in Diabetes Management
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International Journal of Research and Review www.ijrrjournal.com E-ISSN: 2349-9788; P-ISSN: 2454-2237 Review Article Role of Beta-Glucan in Diabetes Management Ambreen Fatima, Reema Verma Lecturer (Home Science), Jhunjhunwala P.G. College & PhD Scholar, SHIATS, Allahabad, India. Corresponding Author: Ambreen Fatima Received: 23/01/2016 Revised: 28/01/2016 Accepted: 01/02/2016 ABSTRACT Diabetes is a universal metabolic disorder prevalent in world and in India it comprises 7.8% of world diabetic population. Beta cells of islets of Langerhans of pancreas secrete insulin hormone which regulate the cellular intake of glucose in human body. Due to insufficient insulin secretion or insulin in sensitivity or any injury in pancreas impairs cellular glucose intake leads rise in blood sugar level. This condition is called as diabetes. Beta glucan found in foods like barley oats etc is a pro-glucagon molecule which exerts strong insulinotropic effects in vivo. It is a good alternative of diabetic medicine for diabetes patients. Key words: Diabetes, Beta Glucan. INTRODUCTION involves an absolute or relative insulin The aetiology of diabetes in India is arises when the pancreas fails to produce multi factorial and includes genetic factors insulin due to destruction of the pancreatic coupled with environmental influences such beta cells usually resulting from an as obesity associated with rising living autoimmune disorder or deficiency occurs standards, steady urban migration, and life when insulin requirements are increased style changes. More than 80% of people live results in insulin resistance (Bowman and in low and middle income countries. Pattern Russel, 2001). It is generally accepted that of diabetes incidence are related to the beta-cell failure is caused by insulin geographical distribution of diabetes in resistance. It was diagnosed that in diabetic India. According to WHO (2014) in 2000 patients β- cell function may have decreased Indian diabetic population was 31.7 million by up to 80% because of increased oxidative and it is expected to be 79.4 till 2030. It stress is one of the mechanisms by which contributes 7.8% (50.8 million) of world hyperglycaemia damages β- cell (DeFronzo diabetic population. Prevalence of diabetes et al., 2008). Treatments with beta cell– in rural population is one- quarter that of preserving properties are therefore essential urban population for India and other Indian for the management of type 2 diabetes sub- continent country such as Bangladesh, (Standl E., 2007). Glucagon like peptide is a Nepal, Bhutan and Sri Lanka. fragment of proglucagon molecule Diabetes is a group of metabolic (Drucker, 1990). it exerts strong disorders resulting from a defect in insulin insulinotropic effects in vivo (Orskov et al., secretion, insulin action or both (ADA, 1987). β - glucans, are frequently present in 2000). These defects alter glucose uptake by endosperm cell walls of cereals. Both cells and its use within them. Insulin soluble and insoluble beta glucans are facilitates glucose uptake and use. Diabetes International Journal of Research & Review (www.gkpublication.in) 91 Vol.3; Issue: 2; February 2016 present in cereals (Ahlu walia and Ellish target nuclear factor- B. Glucagon-like 1985) peptide-1 (7- 36) amide (glucagon-like insulinotropic peptide, or GLIP) is a DISCUSSION gastrointestinal peptide that potentiates the Glucagon-like peptide-1- (7–36) release of insulin in physiologic amide (GLP-1), a potent gluco-incretin concentrations. We compared the effect of hormone (Fehmann et al., 1995) secreted by an infusion of GLIP twofold with the effect the intestinal L-cells in response to fat meals of an infusion of saline, on the meal-related and carbohydrates is a potentially important release of insulin, glucagon, and drug in the treatment of Type 2 diabetes in somatostatin in normal subjects, nine obese view of its ability to improve insulin patients with non- insulin - dependent secretion in subjects with impaired glucose diabetes mellitus. The blood glucose tolerance and Type 2 diabetes mellitus concentrations in the patients with diabetes (Drucker, 2001). A decline in insulin: were controlled by closed- loop insulin - glucagon ratio would favour mobilization of infusion system (artificial pancreas) during stored nutrients; increased hepatic glucose the infusion of each agent, allowing production from glycogen and from measurement of the meal -related available amino acids would occur at the requirement for exogenous insulin. Result expense of protein synthesis, nitrogen demonstrates that in the normal subjects, the balance would shift towards the negative infusion of GLIP significantly lowered the with increased production of urea, and the meal- related increase in the blood glucose release of free fatty acids and glycerol from concentration and the plasma concentration adipose tissue would also increase. In other of insulin and glucagon. GLIP has an words, high insulin: glucagon ratio would antidiabetogenic effect, and it may therefore favor nutrient storage and protein be useful in the treatment of patients with anabolism, while a low insulin: glucagon NIDDM. Shah. et al (2013) studied that the ratio would favor mobilization of nutrient hypothesis that a lack of suppression of stores and protein catabolism (Unger et al., glucagon causes postprandial 1970). hyperglycemia in subjects with type 2 Furthermore Buteau et al. (2004) diabetes. Nine diabetic subjects ingested 50 investigated on whether glucagon-like g glucose on two occasions. On both peptide-1 protects beta cells against cell occasions, somatostatin was infused at a rate death induced by elevated glucose and/or of 4.3 nmol/kg·min, and insulin was infused non-esterified fatty acids. Human islets and in a diabetic insulin profile. On one INS832/13 cells were cultured at glucose occasion, glucagon was also infused at a concentrations of 5 or 25 mmol/l in the rate of 1.25 ng/kg·min to maintain portal presence or absence of palmitate. Apoptosis glucagon concentrations constant was evaluated by monitoring DNA (nonsuppressed study day). On the other fragmentation and chromatin condensation. occasion, glucagon infusion was delayed by Wild-type and protein kinase B mutants 2 h to create a transient decrease in were over expressed in INS832/13 cells glucagon (suppressed study day). Glucagon using adenoviruses. Nuclear factor-κB DNA concentrations on the suppressed study day binding was assayed by electrophoretic fell to about 70 ng/L during the first 2 h, mobility shift assay. Results revealed that in rising thereafter to approximately 120 ng/L. human pancreatic beta cells and INS832/13 In contrast, glucagon concentrations on the cells demonstrate a potent protective effect nonsuppressed study day remained constant of glucagon-like peptide-1 on beta cell at about 120 ng/L throughout. The decrease gluco-, lipo- and glucolipotoxicity. This in glucagon resulted in substantially lower effect is mediated via protein kinase B (P < 0.001) glucose concentrations on the activation and possibly its downstream suppressed compared with the International Journal of Research & Review (www.gkpublication.in) 92 Vol.3; Issue: 2; February 2016 nonsuppressed study days (9.2 ± processed from proglucagon in two forms, 0.7 vs. 10.9± 0.8 mmol/L) and a lower (P < of 31 and 37 amino acids. We report that the 0.001) rate of release of glucose from smaller of the two glucagon-like peptides glycogen (labeled by infusing galactose). potently increases cAMP levels, insulin On the other hand, flux through the hepatic mRNA transcripts, and insulin release in UDP-glucose pool (and, by implication, cultured rat insulinoma cells. These results glycogen synthesis), measured using the indicate that glucagon-like peptide I is a acetaminophen glucuronide method, did not physiologic modulator of insulin gene differ on the two occasions. Result showed expression. that lack of suppression of glucagon Glucagon like peptide 1 (GLP1) contributes to postprandial hyperglycemia in (736 amide) is a physiological incretin subjects with type 2 diabetes at least in part hormone that is released after nutrient intake by accelerating glycogenolysis. These data from the lower gut and stimulates insulin suggest that agents that antagonize glucagon secretion at elevated plasma glucose action or secretion are likely to be of value concentrations. It was seen that exogenous in the treatment of patients with type 2 GLP1 (736 amide) is an effective means of diabetes. normalizing fasting plasma glucose Likewise Degn. et al (2004) reported concentrations in poorly controlled Type 2 that once-daily dosing with the GLP-1 diabetic patients. The glucose dependence derivative liraglutide for 1 week in of insulinotropic actions of GLP1 (736 individuals with type 2 diabetes results in 1) amide) appears to be retained in such substantially decreased glucose patients (Nauck et al., 1993). Hallfrisch and concentration lasting 24 h and is ascribable Behall (2013) studied that various grains to a relative increase in insulin secretion and and grain products effective in improving decrease in glucagon concentration; 2) insulin resistance or lowering glycemic reduced EGR, as a result of diminished index. The composition of the grain, GLY; and 3) substantially improved AIR including particle size, amount and type of and maximal insulin secretory capacity. fiber, viscosity, amylose and amylopectin During longer lasting treatment, these content all affect the metabolism of promising antidiabetic effects may be carbohydrates