Carnosine decreased oxidation and glycation products in serum and liver of high‐fat diet and low‐dose streptozotocin‐induced diabetic rats

Summary High‐fat diet (HFD) and low‐dose streptozotocin (STZ)‐treated rats provide useful animal model for type II diabetes mellitus. Oxidative stress and advanced glycation end products (AGEs) play a role in the development of diabetic complications. Carnosine (CAR) has anti‐oxidant and anti‐glycat...

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Veröffentlicht in:International journal of experimental pathology 2017-10, Vol.98 (5), p.278-288
Hauptverfasser: Aydın, Abdurrahman Fatih, Bingül, İlknur, Küçükgergin, Canan, Doğan‐Ekici, Işın, Doğru Abbasoğlu, Semra, Uysal, Müjdat
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container_issue 5
container_start_page 278
container_title International journal of experimental pathology
container_volume 98
creator Aydın, Abdurrahman Fatih
Bingül, İlknur
Küçükgergin, Canan
Doğan‐Ekici, Işın
Doğru Abbasoğlu, Semra
Uysal, Müjdat
description Summary High‐fat diet (HFD) and low‐dose streptozotocin (STZ)‐treated rats provide useful animal model for type II diabetes mellitus. Oxidative stress and advanced glycation end products (AGEs) play a role in the development of diabetic complications. Carnosine (CAR) has anti‐oxidant and anti‐glycating properties. We investigated the effects of CAR on oxidation and glycation products in HFD+STZ rats. Rats were fed with HFD (60% of total calories from fat) for 4 weeks, and then a single dose of STZ (40 mg/kg; i.p.) was applied. Rats with blood glucose levels above 200 mg/dl were fed with HFD until the end of the 12th week. CAR (250 mg/kg body weight; i.p.; five times a week) was administered to the rats for the last four weeks. CAR significantly decreased serum triglyceride (TG) (57.7%), cholesterol (35.6%) levels and hepatic marker enzyme activities of HFD+STZ rats. It significantly reduced serum reactive oxygen species (ROS) (23.7%), AGEs (13.4%) and advanced oxidized protein products (AOPP) (35.9%) and hepatic TG (59%), ROS (26%), malondialdehyde (MDA) (11.5%), protein carbonyl (PC) (19.2%) and AGE (20.2%) levels. Liver steatosis and hepatocyte ballooning were also significantly reduced. However, CAR treatment did not alter serum glucose and blood glycated haemoglobin and hepatic anti‐oxidant enzyme activities/mRNA expressions in HFD+STZ rats. Our results indicate that CAR decreased accumulation of oxidation and glycation products, such as MDA, AGE, AOPP and PC in the serum and liver and ameliorated hepatic dysfunction in HFD+STZ rats. This effect may be related to its anti‐oxidative, anti‐glycating, and anti‐lipogenic potential.
doi_str_mv 10.1111/iep.12252
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Oxidative stress and advanced glycation end products (AGEs) play a role in the development of diabetic complications. Carnosine (CAR) has anti‐oxidant and anti‐glycating properties. We investigated the effects of CAR on oxidation and glycation products in HFD+STZ rats. Rats were fed with HFD (60% of total calories from fat) for 4 weeks, and then a single dose of STZ (40 mg/kg; i.p.) was applied. Rats with blood glucose levels above 200 mg/dl were fed with HFD until the end of the 12th week. CAR (250 mg/kg body weight; i.p.; five times a week) was administered to the rats for the last four weeks. CAR significantly decreased serum triglyceride (TG) (57.7%), cholesterol (35.6%) levels and hepatic marker enzyme activities of HFD+STZ rats. It significantly reduced serum reactive oxygen species (ROS) (23.7%), AGEs (13.4%) and advanced oxidized protein products (AOPP) (35.9%) and hepatic TG (59%), ROS (26%), malondialdehyde (MDA) (11.5%), protein carbonyl (PC) (19.2%) and AGE (20.2%) levels. Liver steatosis and hepatocyte ballooning were also significantly reduced. However, CAR treatment did not alter serum glucose and blood glycated haemoglobin and hepatic anti‐oxidant enzyme activities/mRNA expressions in HFD+STZ rats. Our results indicate that CAR decreased accumulation of oxidation and glycation products, such as MDA, AGE, AOPP and PC in the serum and liver and ameliorated hepatic dysfunction in HFD+STZ rats. This effect may be related to its anti‐oxidative, anti‐glycating, and anti‐lipogenic potential.</description><identifier>ISSN: 0959-9673</identifier><identifier>EISSN: 1365-2613</identifier><identifier>DOI: 10.1111/iep.12252</identifier><identifier>PMID: 29205589</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>advanced glycation end products ; Advanced glycosylation end products ; Animals ; Antioxidants - pharmacology ; Blood ; Blood Glucose - metabolism ; Body weight ; Body Weight - drug effects ; Calories ; Carbonyls ; Carnosine ; Carnosine - pharmacology ; Cholesterol ; Cholesterol - blood ; Complications ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental - etiology ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Experimental - pathology ; Diabetes Mellitus, Type 2 - etiology ; Diabetes Mellitus, Type 2 - metabolism ; Diabetes Mellitus, Type 2 - pathology ; Diet, High-Fat ; Drug Evaluation, Preclinical - methods ; Enzymes ; Fatty liver ; Glucose ; Glycated Hemoglobin A - metabolism ; Glycation End Products, Advanced - metabolism ; Glycosylation ; Hemoglobin ; High fat diet ; Liver ; Liver - metabolism ; Liver - pathology ; Liver diseases ; Male ; Malondialdehyde ; mRNA ; Organ Size - drug effects ; Original ; Oxidation ; Oxidation-Reduction - drug effects ; Oxidative stress ; Oxidative Stress - drug effects ; Rats ; Rats, Wistar ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Rodents ; Steatosis ; Streptozocin ; Triglycerides - blood</subject><ispartof>International journal of experimental pathology, 2017-10, Vol.98 (5), p.278-288</ispartof><rights>2017 The Authors. International Journal of Experimental Pathology © 2017 International Journal of Experimental Pathology</rights><rights>2017 The Authors. International Journal of Experimental Pathology © 2017 International Journal of Experimental Pathology.</rights><rights>International Journal of Experimental Pathology © 2017 International Journal of Experimental Pathology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5092-1501d3254d72a9a29cfc3872b2906cdcb496d1c421eca648dfbee6b7c113d9bd3</citedby><cites>FETCH-LOGICAL-c5092-1501d3254d72a9a29cfc3872b2906cdcb496d1c421eca648dfbee6b7c113d9bd3</cites><orcidid>0000-0002-2595-0833</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5743804/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5743804/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,27901,27902,45550,45551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29205589$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aydın, Abdurrahman Fatih</creatorcontrib><creatorcontrib>Bingül, İlknur</creatorcontrib><creatorcontrib>Küçükgergin, Canan</creatorcontrib><creatorcontrib>Doğan‐Ekici, Işın</creatorcontrib><creatorcontrib>Doğru Abbasoğlu, Semra</creatorcontrib><creatorcontrib>Uysal, Müjdat</creatorcontrib><title>Carnosine decreased oxidation and glycation products in serum and liver of high‐fat diet and low‐dose streptozotocin‐induced diabetic rats</title><title>International journal of experimental pathology</title><addtitle>Int J Exp Pathol</addtitle><description>Summary High‐fat diet (HFD) and low‐dose streptozotocin (STZ)‐treated rats provide useful animal model for type II diabetes mellitus. Oxidative stress and advanced glycation end products (AGEs) play a role in the development of diabetic complications. Carnosine (CAR) has anti‐oxidant and anti‐glycating properties. We investigated the effects of CAR on oxidation and glycation products in HFD+STZ rats. Rats were fed with HFD (60% of total calories from fat) for 4 weeks, and then a single dose of STZ (40 mg/kg; i.p.) was applied. Rats with blood glucose levels above 200 mg/dl were fed with HFD until the end of the 12th week. CAR (250 mg/kg body weight; i.p.; five times a week) was administered to the rats for the last four weeks. CAR significantly decreased serum triglyceride (TG) (57.7%), cholesterol (35.6%) levels and hepatic marker enzyme activities of HFD+STZ rats. It significantly reduced serum reactive oxygen species (ROS) (23.7%), AGEs (13.4%) and advanced oxidized protein products (AOPP) (35.9%) and hepatic TG (59%), ROS (26%), malondialdehyde (MDA) (11.5%), protein carbonyl (PC) (19.2%) and AGE (20.2%) levels. Liver steatosis and hepatocyte ballooning were also significantly reduced. However, CAR treatment did not alter serum glucose and blood glycated haemoglobin and hepatic anti‐oxidant enzyme activities/mRNA expressions in HFD+STZ rats. Our results indicate that CAR decreased accumulation of oxidation and glycation products, such as MDA, AGE, AOPP and PC in the serum and liver and ameliorated hepatic dysfunction in HFD+STZ rats. 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Oxidative stress and advanced glycation end products (AGEs) play a role in the development of diabetic complications. Carnosine (CAR) has anti‐oxidant and anti‐glycating properties. We investigated the effects of CAR on oxidation and glycation products in HFD+STZ rats. Rats were fed with HFD (60% of total calories from fat) for 4 weeks, and then a single dose of STZ (40 mg/kg; i.p.) was applied. Rats with blood glucose levels above 200 mg/dl were fed with HFD until the end of the 12th week. CAR (250 mg/kg body weight; i.p.; five times a week) was administered to the rats for the last four weeks. CAR significantly decreased serum triglyceride (TG) (57.7%), cholesterol (35.6%) levels and hepatic marker enzyme activities of HFD+STZ rats. It significantly reduced serum reactive oxygen species (ROS) (23.7%), AGEs (13.4%) and advanced oxidized protein products (AOPP) (35.9%) and hepatic TG (59%), ROS (26%), malondialdehyde (MDA) (11.5%), protein carbonyl (PC) (19.2%) and AGE (20.2%) levels. Liver steatosis and hepatocyte ballooning were also significantly reduced. However, CAR treatment did not alter serum glucose and blood glycated haemoglobin and hepatic anti‐oxidant enzyme activities/mRNA expressions in HFD+STZ rats. Our results indicate that CAR decreased accumulation of oxidation and glycation products, such as MDA, AGE, AOPP and PC in the serum and liver and ameliorated hepatic dysfunction in HFD+STZ rats. This effect may be related to its anti‐oxidative, anti‐glycating, and anti‐lipogenic potential.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>29205589</pmid><doi>10.1111/iep.12252</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-2595-0833</orcidid><oa>free_for_read</oa></addata></record>
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source MEDLINE; Wiley Online Library Journals Frontfile Complete; PubMed Central
subjects advanced glycation end products
Advanced glycosylation end products
Animals
Antioxidants - pharmacology
Blood
Blood Glucose - metabolism
Body weight
Body Weight - drug effects
Calories
Carbonyls
Carnosine
Carnosine - pharmacology
Cholesterol
Cholesterol - blood
Complications
Diabetes
Diabetes mellitus
Diabetes Mellitus, Experimental - etiology
Diabetes Mellitus, Experimental - metabolism
Diabetes Mellitus, Experimental - pathology
Diabetes Mellitus, Type 2 - etiology
Diabetes Mellitus, Type 2 - metabolism
Diabetes Mellitus, Type 2 - pathology
Diet, High-Fat
Drug Evaluation, Preclinical - methods
Enzymes
Fatty liver
Glucose
Glycated Hemoglobin A - metabolism
Glycation End Products, Advanced - metabolism
Glycosylation
Hemoglobin
High fat diet
Liver
Liver - metabolism
Liver - pathology
Liver diseases
Male
Malondialdehyde
mRNA
Organ Size - drug effects
Original
Oxidation
Oxidation-Reduction - drug effects
Oxidative stress
Oxidative Stress - drug effects
Rats
Rats, Wistar
Reactive oxygen species
Reactive Oxygen Species - metabolism
Rodents
Steatosis
Streptozocin
Triglycerides - blood
title Carnosine decreased oxidation and glycation products in serum and liver of high‐fat diet and low‐dose streptozotocin‐induced diabetic rats
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