It is well known that posterior capsule opacification (PCO), one of the most common late postoperative complications of cataract surgery, is mainly caused by proliferation and differentiation of remaining lens epithelial cells (LECs) on the posterior lens capsule. Many authors suggest that alterations induced by the pathophysiology of cataracts, its metabolism and the use of 0.1% trypan blue (TB) must cause some degree of cellular damage on these cells, wicht would help to prevent and/or reduce the incidence of PCO after cataract surgery in humans. Therefore, the aim of this study was to evaluate the expression of cell death markers on LECs of older dogs with diabetic and hypermature cataracts, after capsulorhexis, both using 0.1% TB. Twenty samples collected from 13 dogs of different breeds, with ages varying from 8 to 12 years-old, with diabetic and hypermature cataracts, which had been subjected to phacoemulsification surgery (Phaco) using 0.1% TB for staining were studied. Animals were classified as dogs with diabetic (DC) and hypermature cataracts (HC), and expression of molecular markers for apoptosis and autophagy (caspase-3 and beclin-1) on LECs were obtained by immunofluorescence technique. The expression of caspase-3 and beclin-1 was observed in every studied sample and did not differ between groups. In conclusion, our findings suggest that apoptosis and autophagy processes occur to LECs in older dogs presenting diabetic and hypermature cataracts after Phaco utilizing 0.1% TB. Our results may be helpful to future studies of PCO in post-phacoemulsification surgery patients.

Objective: Jicama (Pachyrhizus erosus) fiber has been documented to exert an immunomodu¬latory effect both in vitro and in vivo. However, its beneficial effect against metabolic syndrome remains unknown. This study aimed to reveal whether the jicama fiber (JF) could prevent the development of diabetes and obesity caused by a high-sugar diet (HSD). Materials and Methods: The JF was isolated from its tuberous part and subsequently used as a supplemental diet for adult male Bagg and Albino (BALB)/c mice fed with a HSD. Four different diet paradigms including normal diet, HSD (30% sucrose), and HSD in combination with 10% and 25% of JF, respectively, were deployed continuously for 8 weeks. Furthermore, the blood glucose level, glucose tolerance, body weight, food and water consumption as well as epididymal white adipose tissue (WAT) and interscapular brown adipose tissue (BAT) mass were determined. Results: Our results revealed that supplementation of 25% JF could significantly prevent the blood glucose increase, excessive body weight gain, and glucose intolerance in mice fed with HSD. Moreover, 10% and 25% JF blunted the HSD-induced WAT mass gain but failed to counteract the depletion of BAT mass. Furthermore, the fiber supplementation elicited a minimum effect on rhythm and total food and water intake. Conclusion: The JF could effectively sustain blood glucose homeostasis as well as improve body weight and WAT mass profile against the development of diabetes and obesity caused by HSD. [J Adv Vet Anim Res 2019; 6(2.000): 222-230]

Objectives: Aqueous extracts of Rhizophora mucronata and Avicennia marina leaves were inves¬tigated for their hepatoprotective potential in diabetic rats. Materials and methods: One hundred twenty male albino rats were randomly assigned to eight equal groups (n = 15). The first group (control) comprised normal healthy rats, while the second to fifth groups were intraperitoneally injected with a single dose of streptozotocin (STZ) [60 mg/ kg body weight (BW)] for induction of diabetes. Group 2 was kept as positive diabetic control, while groups 35 were orally treated with aqueous extracts of R. mucronata (400 mg/kg BW), A. marina (400 mg/kg BW) and with a combination of ½ a dose of the two plants, respectively, for six weeks. Groups 68 were non-diabetic rats that orally received aqueous extracts of R. mucronata (400 mg/kg BW), A. marina (400 mg/kg BW), and a combination of ½ a dose of the two plants, respectively, for 6 weeks. Results: STZ-induced diabetic rats showed a significant reduction in serum glucose and liver enzymes, increased serum insulin, Homeostasis Model Assessment of β-cells (HOMA-β), and Homeostasis Model Assessment of Insulin Resistance (HOMA-IR). Histopathological and immuno¬histochemical examinations of the liver revealed improved pathologic criteria in the plant extract treated diabetic rats compared with the remarkable changes which had been seen in STZ-induced diabetic rats. Conclusion: This study suggests that the aqueous extract of R. mucronata or its combination with A. marina showed potent hypoglycemic and hepatoprotective effects for liver dysfunction, as well as histopathological and immunohistochemical changes in the liver of STZ-induced diabetic rats. [J Adv Vet Anim Res 2020; 7(1.000): 177-185]

Diabetes is a series of metabolic conditions which threaten public health, caused by a defect in insulin secretion by the pancreatic β-cells or insulin-sensitive tissues that fail to respond to insulin leads to hyperglycemia, which causes a series of metabolic signaling pathways leading to inflammation, cytokine production, cell death, and diabetic complications. Recent research has pointed to Histidine-containing dipeptides (HDPs) to be one of the routes to enhancing diabetic complications. HDPs are synthesized in muscle and are abundantly found in mammals and other vertebrates. L-carnosine (CAR), Anserine, and homocarnosine are dipeptides produced by vertebrate muscles. Carnosine and anserine have both antiglycation and antioxidant activity that help to enhance metabolic dysregulation caused by diabetes. In addition, homocarnosine has anti-inflammatory activity, as well as the ability to reduce DNA damage and advanced glycation end products (AGEs). This review will focus on the protective effects of HDPs against diabetic complications, especially carnosine.