PMID- 30021358 OWN - NLM STAT- MEDLINE DCOM- 20181102 LR - 20181102 IS - 1950-6007 (Electronic) IS - 0753-3322 (Linking) VI - 105 DP - 2018 Sep TI - Therapeutic effect of vitamin B(3) on hyperglycemia, oxidative stress and DNA damage in alloxan induced diabetic rat model. PG - 1223-1231 LID - S0753-3322(18)32878-6 [pii] LID - 10.1016/j.biopha.2018.06.085 [doi] AB - Evidences in the form of experimental analysis and scientific investigations suggest that oxidative stress embody an imperative role in the onset and progression of type-2 diabetes mellitus (T2DM). Aberrant elevation in levels of free radicals, as observed upon disease onset, and the subsequent reduction in anti-oxidant defenses is pernicious to metabolic enzymes and cellular organelles. Niacin (Vitamin B(3)) is an essential nutrient for humans and is considered to be an important food additive for animals too. This research was conducted to examine the effect of nutraceutical antioxidant on diabetic environment. This important member of Vitamin B complex is a forerunner of nicotinamide adenine dinucleotide (NAD) and also nicotinamide adenine dinucleotide phosphate (NADP), both of them serving as coenzymes for several metabolic enzymes. This study reports the effects of niacin supplementation in alloxan induced diabetic rats divided into five groups. Diabetes induced rats were further treated with niacin at two doses (10 and 15 mg /kg body weight) and compared with a control set of diabetes without treatment. Niacin treatment showed recovery in almost all parameters in a dose reliant pattern. A notable decline in oxidative stress parameters with reductions in fasting blood glucose levels was observed. Histological studies reveal damage recovery in the liver as well as kidney tissues. A notable amount of recovery was observed in cellular DNA damage. As a deduction, it is advocated that dietary niacin supplementation might help in reducing problems associated with diabetes. A probable mechanism pertaining to the action of niacin is proposed as well. CI - Copyright (c) 2018 Elsevier Masson SAS. All rights reserved. FAU - Abdullah, K M AU - Abdullah KM AD - Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim University, Aligarh 202002, India. FAU - Alam, Md Maroof AU - Alam MM AD - Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim University, Aligarh 202002, India. FAU - Iqbal, Zarmin AU - Iqbal Z AD - Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim University, Aligarh 202002, India. FAU - Naseem, Imrana AU - Naseem I AD - Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim University, Aligarh 202002, India. Electronic address: imrananaseem2009@gmail.com. LA - eng PT - Journal Article DEP - 20180622 PL - France TA - Biomed Pharmacother JT - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie JID - 8213295 RN - 0 (Antioxidants) RN - 0 (Blood Glucose) RN - 25X51I8RD4 (Niacinamide) RN - 6SW5YHA5NG (Alloxan) SB - IM MH - Alloxan/*pharmacology MH - Animals MH - Antioxidants/pharmacology MH - Blood Glucose/drug effects MH - DNA Damage/*drug effects MH - Diabetes Mellitus, Experimental/blood/*chemically induced/*drug therapy MH - Diabetes Mellitus, Type 2/blood/chemically induced/drug therapy MH - Dietary Supplements MH - Hyperglycemia/*drug therapy MH - Liver/drug effects MH - Male MH - Niacinamide/*pharmacology MH - Oxidative Stress/*drug effects MH - Rats MH - Rats, Wistar OTO - NOTNLM OT - Alloxan OT - Diabetes OT - Hyperglycemia OT - Vitamin B3 EDAT- 2018/07/20 06:00 MHDA- 2018/11/06 06:00 CRDT- 2018/07/20 06:00 PHST- 2018/04/30 00:00 [received] PHST- 2018/06/14 00:00 [revised] PHST- 2018/06/14 00:00 [accepted] PHST- 2018/07/20 06:00 [entrez] PHST- 2018/07/20 06:00 [pubmed] PHST- 2018/11/06 06:00 [medline] AID - S0753-3322(18)32878-6 [pii] AID - 10.1016/j.biopha.2018.06.085 [doi] PST - ppublish SO - Biomed Pharmacother. 2018 Sep;105:1223-1231. doi: 10.1016/j.biopha.2018.06.085. Epub 2018 Jun 22.