COMPARATIVE EFFECT OF A HIGH FAT WITH OR WITHOUT HIGH LEVELS OF SUCROSE DIETS ON PERIPHERAL NEUROPATHY IN C57BL/6J MICE.
diet induced obesity
high fat and high sucrose diet
peripheral neuropathy
type 2 diabetes
western diet
Journal
Journal of diabetic complications & therapy
Titre abrégé: J Diabet Complicat Ther
Pays: United States
ID NLM: 9918366787406676
Informations de publication
Date de publication:
2022
2022
Historique:
medline:
1
1
2022
pubmed:
1
1
2022
entrez:
19
6
2023
Statut:
ppublish
Résumé
Feeding mice a diet containing high fat and high sucrose has been promoted as a good model for type 2 diabetes. This study sought to determine the effect of feeding mice a high fat and high sucrose diet on neuropathy compared to mice fed only a high fat diet and mice fed a high diet and treated with streptozotocin. C57Bl/6J mice were divided into five groups and fed the following diets for 20 weeks: Normal (Control); Sucrose enriched (Control + Sucrose), High Fat (Diet-induced obesity (DIO)), High Fat and High Sucrose (DIO + sucrose) and High Fat diet/streptozotocin treated (Diabetic). The endpoints evaluated included motor and sensory nerve conduction velocity, thermal and mechanical sensitivity and innervation of sensory nerves in the cornea and skin. Diabetic mice were hyperglycemic at the end of the study and along with DIO mice with or without Sucrose had impaired glucose utilization. DIO mice had slowed sensory nerve conduction velocity, mechanical allodynia and decreased innervation of the cornea and skin. DIO + Sucrose and to a greater extent diabetic mice were thermal hypoalgesic, had mechanical allodynia, reduced motor and sensory nerve conduction velocities and decrease innervation of the cornea and skin. Development of peripheral neuropathy was more severe in High Fat and High Sucrose fed mice compared to high fat fed mice but fasting hyperglycemia and impaired glucose utilization was similar for these two models. Peripheral neuropathy was most severe in diabetic mice.
Identifiants
pubmed: 37332358
pmc: PMC10274354
mid: NIHMS1786243
pii:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : RRD VA
ID : I01 RX000889
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK107399
Pays : United States
Références
Diabetes. 2015 Jun;64(6):2254-64
pubmed: 25552598
Sci Rep. 2016 May 27;6:26933
pubmed: 27230286
Free Radic Res. 2017 Apr;51(4):360-367
pubmed: 28376643
Neuropharmacology. 2011 Feb-Mar;60(2-3):259-66
pubmed: 20849865
Exp Eye Res. 2017 Sep;162:104-109
pubmed: 28757158
Biomedicines. 2020 Aug 28;8(9):
pubmed: 32872256
J Peripher Nerv Syst. 2014 Sep;19(3):205-17
pubmed: 25403729
Phytother Res. 2019 Sep;33(9):2347-2359
pubmed: 31273855
Exp Diabetes Res. 2009;2009:431980
pubmed: 20148083
Diabetes Metab Res Rev. 2014 Nov;30(8):669-78
pubmed: 24687457
J Nutr Metab. 2016;2016:5905891
pubmed: 27774316
J Diabetes Res. 2021 Mar 15;2021:5564477
pubmed: 33816635
Diabetes Metab Res Rev. 2010 May;26(4):306-18
pubmed: 20503263
Front Physiol. 2018 Sep 05;9:1054
pubmed: 30258366
Hepatology. 2013 Nov;58(5):1632-43
pubmed: 23813872
J Diabetes Res. 2016;2016:2902351
pubmed: 27547764
Methods Mol Biol. 2016;1438:153-75
pubmed: 27150090
Diabetologia. 2003 May;46(5):683-8
pubmed: 12739016
Diabetes Metab Syndr Obes. 2020 Apr 24;13:1367-1384
pubmed: 32425569
J Neuropathol Exp Neurol. 2016 Nov 1;75(11):1072-1080
pubmed: 27634964
ILAR J. 2014;54(3):259-72
pubmed: 24615439
Invest Ophthalmol Vis Sci. 2014 Mar 03;55(3):1222-30
pubmed: 24519423
Neuropharmacology. 2017 Apr;116:122-131
pubmed: 28025096
Int Rev Neurobiol. 2016;127:89-112
pubmed: 27133146
J Mol Cell Cardiol. 2015 Jan;78:165-73
pubmed: 25109264
J Neurophysiol. 2015 Jul;114(1):199-208
pubmed: 25925322
Sci Rep. 2019 Dec 20;9(1):19556
pubmed: 31862918
Curr Protoc Mouse Biol. 2016 Sep 01;6(3):223-255
pubmed: 27584552
J Cardiovasc Magn Reson. 2015 Nov 06;17:95
pubmed: 26546347
Diabetes Metab Syndr Obes. 2018 Apr 09;11:117-127
pubmed: 29674850
J Peripher Nerv Syst. 2015 Mar;20(1):24-31
pubmed: 25858759
Physiol Rep. 2018 Jun;6(11):e13729
pubmed: 29890051