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Mohamed H Noureldein, Sara Bitar, Natalie Youssef, Sami Azar, and Assaad A Eid

Diabetic dysbiosis has been described as a novel key player in diabetes and diabetic complications. However, the cellular/molecular alterations associated with dysbiosis remain poorly characterized. For that, control, non-obese type 2 diabetic MKR mice and MKR mice treated with butyrate were used to delineate the epigenetic, cellular and molecular mechanisms by which dysbiosis associated with diabetes induces colon shortening and inflammation attesting to gastrointestinal disturbance. Our results show that dysbiosis is associated with T2DM and characterized by reduced Bacteroid fragilis population and butyrate-forming bacteria. The reduction of butyrate-forming bacteria and inadequate butyrate secretion result in alleviating HDAC3 inhibition and altering colon permeability. The observed changes are also associated with an increase in ROS production, a rise in NOX4 proteins, and a shift in the inflammatory markers, where IL-1β is increased and IL-10 and IL-17α are reduced. Treatment with butyrate restores the homeostatic levels of NOX4 and IL-1β. In summary, our data suggest that in T2DM, dysbiosis is associated with a reduction in butyrate content leading to increased HDAC3 activity. Butyrate treatment restores the homeostatic levels of the inflammatory markers and reduces ROS production known to mediate diabetes-induced colon disturbance. Taken together, our results suggest that butyrate could be a potential treatment to attenuate diabetic complications.

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Vivek Madhukar Surse, Jeena Gupta, and Kulbhushan Tikoo

K Rimbach G 2001 Molecular aspects of lipoic acid in the prevention of diabetes complications . Nutrition 17 888 – 895 . doi:10.1016/S0899-9007(01)00658-X . Panchapakesan U Sumual S Pollock CA Chen X 2005 PPAR {gamma} agonists

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Sarah X Zhang, Joshua J Wang, Azar Dashti, Kenneth Wilson, Ming-Hui Zou, Luke Szweda, Jian-Xing Ma, and Timothy J Lyons

2005 Aldose reductase inhibition counteracts oxidative-nitrosative stress and poly(ADP-ribose) polymerase activation in tissue sites for diabetes complications . Diabetes 54 234 – 242 . Qaum T Xu Q Joussen AM Clemens MW Qin W Miyamoto

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Rachel Njeim, William S Azar, Angie H Fares, Sami T Azar, Hala Kfoury Kassouf, and Assaad A Eid

118 1952 – 1961 . ( https://doi.org/10.1182/blood-2011-03-343061 ) Skyler JS 2004 Effects of glycemic control on diabetes complications and on the prevention of diabetes . Clinical Diabetes 22 162 – 166 . ( https://doi.org/10

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Young Sun Kang, Yun Gyu Park, Bo Kyung Kim, Sang Youb Han, Yi Hwa Jee, Kum Hyun Han, Mi Hwa Lee, Hye Kyoung Song, Dae Ryong Cha, Shin Wook Kang, and Dae Suk Han

) in glomerular mesangial cells. Journal of Diabetes Complications 9 255 –261.

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Pabitra B Pal, Himangshu Sonowal, Kirtikar Shukla, Satish K Srivastava, and Kota V Ramana

function ( Tabit et al. 2010 , Pitocco et al. 2013 , Shukla et al. 2018 ). Endothelial dysfunction in diabetes has been reported to be associated with the onset of secondary diabetes complications and micro- and macro-vascular diseases ( Hadi

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Bo Li, Yue Zhou, Jing Chen, Tingting Wang, Zhijuan Li, Yili Fu, Aixia Zhai, and Changlong Bi

CTGF in various diabetes complications. Taken together, the aforementioned findings provided evidence that CTGF is poorly expressed in DFU. Additionally, overexpression of CTGF activated the MAPK signaling pathway to promote fibroblast proliferation