Effect of L-Carnitine on Insulin Sensitivity and Responsiveness in Skeletal Muscle, Adipose tissue and Hepatic tissues
Mohammed
Adel
Department of Medical Physiology, Faculty of Medicine, Mansoura University, Egypt
author
text
article
2015
eng
Background and objectives: L-carnitine (LC) is a non-protein amino acid includes both diet and endogenous synthesis. There are no studies on the effect of LC on glucose uptake and net glucose output in muscle and hepatic tissues. So, the aim of the present work is to study the metabolic aspects of LC and to study some mechanisms that may be of help in treatment of insulin resistance. Methods: Twenty four male rats were divided into two main groups, twelve rats per each group. In vivo group was divided into control one and L-Carnitine - treated one, It was given in the dose of 3 gm carnitine/kg once every day orally for 4 weeks where fasting serum glucose and plasma free fatty acids (FFA) were measured. In vitro group included experiments on epididymal fat pad (EFP), hemidiaphragm and liver. Results: LC caused a highly significant decrease in fasting plasma FFA level (4.9 ± 1.5 mg/ dl). However, it caused a significant increase in insulin-stimulated glucose uptake by EFP in the presence of supraminimal and supramaximal insulin concentrations (2.5 ± 0.8 and 3.4± 0.4) (mg/ gm wet tissue /hour) and also by hemidiaphragm (4.9 ± 0.3 and 6 ± 0.97) (mg/ gm wet tissue /hour). Also, it increased net glucose output by liver slices in the presence of both insulin concentrations (- 4.9 ± 1.1 and – 4 ± 1.42) (mg/ gm wet tissue /hour). It decreased FFA release from EFP in the presence of both insulin concentrations (0.5 ± 0.21 and 0.4 ± 0.2 ) (mg/ gm wet tissue /hour), hemidiaphragm (0.5± 0.1 and 0.5 ±0.16) (mg/ gm wet tissue /hour) and liver slices (0.58 ± 0.19 and 0.63± 0.27) (mg/ gm wet tissue /hour). Conclusion: LC increased plasma FFA level. It potentiated the effect of insulin on glucose uptake in EFP and hemidiaphragm. It decreased hepatic insulin sensitivity and responsivity and enhanced the suppressive effect of insulin on FFA release from different peripheral tissues.
Bulletin of Egyptian Society for Physiological Sciences
Egyptian Society for Physiological Sciences
1110-0842
35
v.
2
no.
2015
46
56
https://besps.journals.ekb.eg/article_28995_7d3ce454a27e57131038bae8cb82efae.pdf
dx.doi.org/10.21608/besps.2015.28995
Remedial Effects of Resveratrol on Chronic Unpredictable Stress-Induced Gastric Lesions in Male Albino Rats
Ismaeel
Bin-Jaliah
Department of Physiology, College of Medicine, King Khalid University, Abha, Saudi Arabia
author
text
article
2015
eng
Objectives: Stress of various patterns has been linked to pathologies of body organs, including gastric mucosal damage. The polyphenol Resveratrol (RES) has been reported to have anti-ulcer properties against some models of gastric ulcer. However, its effect against experimental chronic unpredictable stress (CUS)-induced ulcer per se was not studied before. This study aims to investigate the gastric mucosal damage induced by CUS, its potential prevention by RES, and the mechanisms of action implicated. Methods. Thirty two rats were randomized into 4 groups, 8 rats each: Control, Control+ RES, CUS, and CUS+RES. The CUS was applied for 3 weeks, during which the vehicle (Normal Saline) or RES (25 mg.kg-1) was intraperitoneally administered on daily doses. Ulceration index, oxidative, inflammatory and apoptotic parameters were measured. Results. CUS induced severe gastric lesions of various extents, with considerable erosive microscopic features. There was significant increase in the levels of TBARS, TNF-α, IL-6, Bax and caspase-3 with concomitant significant decrease in the levels of SOD, GPX, PGE2, and Bcl-2 in CUS rats compared to control rats. Resveratrol treatment to CUS stressed rats brought all of these parameters to control levels, and remarkably maintained the normal morphology and microscopic architectures of gastric tissue. Conclusion. The present data show that supplementation with resveratrol ameliorates CUS-induced gastric lesions via its antioxidant, anti-inflammatory and anti-apoptotic potentials; a promising protective consequence that may demand further exploration.
Bulletin of Egyptian Society for Physiological Sciences
Egyptian Society for Physiological Sciences
1110-0842
35
v.
2
no.
2015
57
72
https://besps.journals.ekb.eg/article_28996_7477b0212555401ed87177cd61ca3958.pdf
dx.doi.org/10.21608/besps.2015.28996
The potential protective effects of tetrahydrobiopterin on cadmium-induced pancreatic changes in male rats
Ebtihal
Abd EL-Aziz
Department of Physiology. Faculty of Medicine. Assiut University. Egypt.
author
Nashwa
Abd El-Mottaleb
Department of Physiology. Faculty of Medicine. Assiut University. Egypt.
author
text
article
2015
eng
Cadmium (Cd) is a widespread environmental and industrial pollutant. It accumulates in the pancreas and could influence its endocrine and exocrine functions. Tetrahydrobiopterin (BH4) is essential for various processes, and present in all tissues of higher organisms. This study was designed to investigate the effect of BH4 on the acute pancreatic damage induced by Cd and detect its mechanism(s) of action. Thirty rats were randomly divided into three groups (10 rats each). Control : received saline, Cd: received (single dose of CdCl2 4 mg/kg, i.p.) and BH4+Cd : received (single dose of BH4 20 mg/kg, i.p.) one hour before single dose of CdCl2 (4 mg/kg, i.p.). The α-amylase, lipase, glucose, insulin and interleukin 6 (IL-6) levels were measured in serum and intercellular adhesion molecule-1(ICAM-1), malondialdehyde (MDA) and superoxide dismutase (SOD) levels were measured in pancreatic homogenate. Histopathological examination of pancreas was done. BH4 improved pancreatic functions, where α-amylase, lipase, glucose and IL-6 levels were significantly decreased while insulin levels were significantly increased in serum. Pancreatic damage was ameliorated as evident by significant decrease of ICAM-1 and MDA and significant increase of SOD levels in pancreatic homogenate. Also, the disturbed pancreatic tissues were ameliorated. In conclusion, BH4 induced improvements in pancreatic tissue and functions in cadmium-exposed rats. Part of BH4 beneficial effects could be attributed to anti-oxidative and anti-inflammatory activity
Bulletin of Egyptian Society for Physiological Sciences
Egyptian Society for Physiological Sciences
1110-0842
35
v.
2
no.
2015
73
85
https://besps.journals.ekb.eg/article_34478_f43cbe8ce052d358c0c336664bcbf0e2.pdf
dx.doi.org/10.21608/besps.2015.34478
Effects of vitamin d3 on ppar-α and its target gene nfkbia on a rat model of high carbohydrate high fat diet induced non alcoholic steatohepatitis
Mohamed
El-Dosoky
Department of Medical Physiology, Faculty of Medicine, Mansoura University, Egypt
author
Sally
Abed
Department of Tropical Medicine, Faculty of Medicine, Mansoura University, Egypt
author
Mohamed
Elshafey
Department of Human Anatomy and Embryology, Faculty of Medicine, Mansoura University, Egypt
author
text
article
2015
eng
Accumulating data suggesting that Vitamin D3 could be of a potential therapeutic value for non-alcoholic fatty liver disease (NAFLD) ,but its underlying mechanisms are still under research .Vitamin D3 up regulates PPAR-α and downstream gene nuclear factor-kappa-B inhibitor subunit-alpha (NFKBIA) which may represent a novel strategy for the management of NASH. Therefore, in this study, we investigated the possible protective role of vitamin D3 on high carbohydrate high fat diet (HCHFD) animal model of NASH through PPAR-α and NFKBIA pathway Methods: Thirty male Sprague-Dawley rats were equally divided into three groups; group I: (negative control group) fed standard rat chow diet for 8 weeks. group II: received HCHFD for 8 weeks. group III: fed as group II for 8 weeks and received also, I.P administration of vitamin D3 at a dose of 5 μg/kg twice weekly from the fourth week till the end of the study. At the end of the experiment, serum triglycerides, total cholesterol, liver enzymes, serum albumin, serum bilirubin and liver tissue oxidative stress markers (MDA, SOD and GSH) were measured. Hepatic histopathological alterations were assessed by hematoxylin and eosin, Masson’s trichrome, and Oil Red O staining ; the expressions of NF-κ B p65 (ReIA) was estimated in liver tissues using immunohistochemistry and the expression of hepatic PPAR-α and NFKBIA genes were estimated at the level of mRNA by quantitative real-time PCR. Results: Nonalcoholic steatohepatitis (NASH) model was confirmed by histopathological examination as indicated by elevated NAFLD activity score (NAS) as well as elevation of serum liver enzymes , hyperlipidemia in the form elevated plasma triglycerides and total cholesterol, oxidative stress state (high MDA, low GSH and SOD) and down regulation of PPAR-α and NFKBIA mRNA in liver tissues which was concomitant with up regulation of inflammatory marker NF-κ B-p65(ReIA) . On the other hand, vitamin D3 ameliorated NASH by attenuation of oxidative stress (low MDA, high GSH and SOD) and up regulation of PPAR-α and NFKBIA genes at the level of mRNA in the liver tissues which was accompanied by decrease in hepatocyte nuclear NF-κ B-p65 (ReIA) immunohistochemical brownish staining. Conclusion: Vitamin D3 attenuates NASH in HCHFD rat model by attenuation of redox state and up regulation of PPAR-α and its downstream gene NFKBIA in liver tissues.
Bulletin of Egyptian Society for Physiological Sciences
Egyptian Society for Physiological Sciences
1110-0842
35
v.
2
no.
2015
86
105
https://besps.journals.ekb.eg/article_34482_96ffc2912f706c15a91831676147ca25.pdf
dx.doi.org/10.21608/besps.2015.34482