Immunolocalization of nestin in pancreatic tissue of mice at different ages

Dorisetty, Raj K; Kiran, Sashi G; Umrani, Malathi R; Boindala, Sesikeran; Bhonde, Ramesh; Venkatesan, Vijayalakshmi

doi:10.3748/wjg.14.7112

Cited by 9 publications

(11 citation statements)

References 26 publications

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“…Here, we found that GLP1R KD ΔNestin are highly resistant to the food intake and body weight lowering effects of liraglutide, supporting an important role for CNS GLP1R in mediating these effects. It should be noted that Cre driven by the nestin promoter has been widely used for loss-of-function of specific genes in the CNS, but it is expressed in other tissues, as evidenced by the reduced GLP1R in the pancreas of GLP1R KD ΔNestin animals (11,12). However, it is unlikely that other tissues targeted by nestin are likely to make large contributions to the effects of GLP1 analogs on these behavioral end points.…”

Section: Discussionmentioning

confidence: 99%

Neuronal GLP1R mediates liraglutide’s anorectic but not glucose-lowering effect

et al. 2014

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Glucose control and weight loss are cornerstones of type 2 diabetes treatment. Currently, only glucagon-like peptide-1 (GLP1) analogs are able to achieve both weight loss and glucose tolerance. Both glucose and body weight are regulated by the brain, which contains GLP1 receptors (GLP1R). Even though the brain is poised to mediate the effects of GLP1 analogs, it remains unclear whether the glucose-and body weight-lowering effects of long-acting GLP1R agonists are via direct action on CNS GLP1R or the result of downstream activation of afferent neuronal GLP1R. We generated mice with either neuronal or visceral nerve-specific deletion of Glp1r and then administered liraglutide, a long-acting GLP1R agonist. We found that neither reduction of GLP1R in the CNS nor in the visceral nerves resulted in alterations in body weight or food intake in animals fed normal chow or a high-fat diet. Liraglutide treatment provided beneficial glucose-lowering effects in both chow-and high-fat-fed mice lacking GLP1R in the CNS or visceral nerves; however, liraglutide was ineffective at altering food intake, body weight, or causing a conditioned taste aversion in mice lacking neuronal GLP1R. These data indicate that neuronal GLP1Rs mediate body weight and anorectic effects of liraglutide, but are not required for glucose-lowering effects.

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Section: Discussionmentioning

confidence: 99%

Neuronal GLP1R mediates liraglutide’s anorectic but not glucose-lowering effect

et al. 2014

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“…Immunohistochemical analysis was carried out using the primary polyclonal antiserum (Goat polyclonal anti Cox-2, 1:250, Santa Cruz, USA), and secondary antibody (FITC labeled Donkey anti goat - 1:500, Molecular probes, U.S.A) [17]. Images were captured on Nikon Eclipse microscope (TE 2000-S series) and the fluorescence intensity units (FIU) were corrected using appropriate controls (Primary antibody controls).…”

Section: Methodsmentioning

confidence: 99%

Recombinant Human Epidermal Growth Factor Alleviates Gastric Antral Ulcer Induced by Naproxen: A Non-steroidal Anti Inflammatory Drug

et al. 2010

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BackgroundTo study the effect (s) of recombinant human Epidermal Growth Factor (rhEGF) on naproxen induced gastric ulcer in Wistar NIN rats.MethodsMale Wistar NIN rats were randomly divided into six experimental groups: Group I - Control, Group II - Naproxen treated, Group III - Naproxen with rhEGF/7 days, Group IV - Naproxen without rhEGF/7 days, Group V - Naproxen with rhEGF/14 days, and Group VI - Naproxen without rhEGF/14 days. Gastric ulcer was induced with naproxen at a concentration of 80 mg/kg by oral administration. After 24 hours of induction of ulcer, rhEGF treatment was started at a concentration of 100 µg/kg. Ulcer presence and healing were confirmed by histopathology study and molecular markers.ResultsNaproxen per se induced gastric antral ulcers in Wistar NIN rats. Compared with control rats, naproxen induced rats had increased lipid peroxide content in serum. Subsequent decrease in lipid peroxide was observed in rhEGF treated groups. Treatment with rhEGF significantly resulted in healing of the ulcers, which was evident by 7 days of rhEGF treatment with total healing seen by 14 days. Significant increase in immunoreactivity for Cox-2 was observed when compared to control groups, whereas less immunoreactivity of Cox-2 was observed in rhEGF treated group. Compared with control group, naproxen induced group exhibited more gene expression of both Cox-2 and TGF beta while gene expression of Cox-2 and TGF beta in rhEGF group was comparable to control group.ConclusionsThe beneficial effects of rhEGF in the management of ulcer healing can be understood. Oral rhEGF can promote healing of the rats with gastric ulcer by stimulating Cox-2 and TGF-beta expression.

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“…Homeostasis model of assessment for insulin resistance (HOMA-IR) was calculated using the following formula: Histology In order to perform the pancreatic histopathological study, pancreas were dissected, and processed for hematoxylene and eosin (H&E), Masson's trichome, immunohistochemistry and immune fluorescence using the standard immunohistochemistry protocols. 53 Briefly, formalin fixed, paraffin embedded sections of pancreas were mounted on poly-L lysine coated slides. Sections were dewaxed in xylene and rehydrated through graded ethanol.…”

Section: Plasma and Tissue Insulinmentioning

confidence: 99%

Islet adaptation to obesity and insulin resistance in WNIN/GR-Ob rats

Singh¹,

Ganneru²,

Malakapalli³

et al. 2014

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WNIN/GR-Ob mutant rat is a novel animal model to study metabolic syndrome (obesity, insulin resistance, hyperinsulinemia, impaired glucose tolerance and cardiovascular diseases). We have investigated the islet characteristics of obese mutants at different age groups (1, 6 and 12 months) to assess the islet changes in response to early and chronic metabolic stress. Our data demonstrates altered islet cell morphology and function (hypertrophy, fibrotic lesions, vacuolation, decreased stimulation index, increased TNFa, ROS and TBARS levels) in mutants as compared to controls. Furthermore, network analysis (gene-gene interaction) studied in pancreas demonstrated increased inflammation as a key factor underlying obesity/metabolic syndrome in mutants. These observations pave way to explore this model to understand islet adaptation in response to metabolic syndrome.

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Immunolocalization of nestin in pancreatic tissue of mice at different ages

Cited by 9 publications

References 26 publications

Neuronal GLP1R mediates liraglutide’s anorectic but not glucose-lowering effect

Neuronal GLP1R mediates liraglutide’s anorectic but not glucose-lowering effect

Recombinant Human Epidermal Growth Factor Alleviates Gastric Antral Ulcer Induced by Naproxen: A Non-steroidal Anti Inflammatory Drug

Islet adaptation to obesity and insulin resistance in WNIN/GR-Ob rats

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