To enhance the insulin release from the beta cells of pancreas though their activation. Therefore, it is presupposed that ALEx could be accountable for potentiation of the pancreatic secretion of insulin from regenerated -cells by inhibiting ATP sensitive K + channels like Glibenclamide for stimulation of insulin from the pancreatic beta cells. Diabetic state is characterized by a severe loss in body weight because of loss or degradation of structural proteins [54]. Due to insulin deficiency there is a marked reduction in the protein content in the muscular tissue due to proteolysis [55]. The reversal in loss of weight in the ALEx treated diabetic rats group exhibited that restoration of the weight loss may be due the reversal of proteolysis, gluconeogenesis and glycogenolysis [56]. In experimental diabetes, there is a marked alteration of the enzymes accountable for glucose metabolism. Persistent hyperglycemia is the PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26024392 major factor responsibleAhmed et al. BMC Complementary and Alternative Medicine 2014, 14:243 http://www.biomedcentral.com/1472-6882/14/Page 14 ofFigure 11 Effect of Albizia Lebbeck Benth. stem bark extract (ALEx) on histological profile of liver in normal, STZ-induced diabetic untreated and STZ-induced diabetic treated wistar rats (Original magnification 40? DXIT 1200 , Nikon, Japan). (i) NLALx: Heamatoxylin and eosin (H/E) stained sections of liver of normal control rats showing normal portal triad along with normal hepatocytes with central vein (Beclabuvir web yellow arrows). (ii) STZL: Liver section of rats received streptozotocin depicting destructed portal trial, disarranged hepatocytes and central vein (yellow arrows).(iii) ALEx100: Section of liver supplemented with 100 mg/kg body wt. of ALEx portaying improvement in structure of portal triad (yellow arrows). (iv)ALEx200: Liver section of rats received 200 mg/kg body wt. of ALEx showing arranged hepatocytes (yellow arrows). (v) ALEx300: Section of liver or diabetic rats treated with 300 mg/kg body wt. of ALEx depicting arranged central vein (yellow arrows). (vi) ALEx400: Liver of diabetic rat showing normal portal traid, central vein and hepatocytes (yellow arrows). (vii) LGLB: Liver section of rat administered with Glibenclamide showing normal microvasculature along with normal hepatocytes (yellow arrows).for such metabolic alterations that lead to the development of diabetic complications such as neuropathy and micro-vascular complications [57]. Hepatic Hexokinase and glucose-6-phosphate dehydrogenase activities have been found to be decreased in the diabetic rats, which may be due to the insufficiency of insulin. Hexokinase is one of the important enzyme responsible for phosphorylation of glucose into glucose-6-phosphate [58]. Insufficiency of hexokinase results in decreased glycolysis and a marked reduction in the utilization of glucose for the production of energy. Oral administration of ALEx to diabetic rats resulted in considerable increase in the activity of hexokinase in dose dependent manner (Table 5). The activities of hepatic glucose-6-phosphatase as well as fructose-1,6 biphosphatase were increased to a significant extent in STZ induced diabetic rats. The above mentioned enzymes are the key regulators in gluconeogenic pathway. The increased activities of the two enzymes may be due to the increased synthesis of enzymes contributing to the enhanced glucose production by the liver in the period of diabetes [59]. In our research exertion, administration of ALEx had a sig.
