Date of Award

2018

Degree Name

Biology

College

College of Science

Type of Degree

M.S.

Document Type

Thesis

First Advisor

Dr. Eric Blough, Committee Chairperson

Second Advisor

Dr. Charles Somerville

Third Advisor

Dr. David Mallory

Fourth Advisor

Dr. Nandini Manne

Abstract

Metabolic syndrome is one of the fastest growing health problems in the world. The medical costs associated with treating this disorder are staggering. Allowed to proceed untreated, metabolic syndrome can lead to a markedly decreased quality of life and a variety of medical conditions including heart and kidney failure. Whether the sodium glucose co-transporter-2 (SGLT-2) inhibitor Empagliflozin can be used to prevent the development of metabolic syndrome is not well understood. This proposal is specifically designed to address this gap in our knowledge. The expected outcomes of this work will identify the time course and degree of interrelatedness between changes in insulin sensitivity / obesity, alterations in expression of the mitogen activated protein kinases (MAPK), and the effects of Empagliflozin treatment on these parameters in the fast twitch extensor digitorium longus (EDL) and the slow-twitch soleus muscles in lean and obese Zucker rats. Male five-week-old lean and obese Zucker rats were randomly assigned to one of the four groups- lean control, lean treated, obese control, and obese treated. Animals were treated with either Empagliflozin (10 mg/kg BW / day) or placebo for 25 weeks. Compared to that seen in the obese controls, Empagliflozin treatment in the obese animals was associated with decreased body weight and improvements in glucose tolerance. Empagliflozin treatment did not appear to affect EDL or soleus muscle weight or the expression of ERK1/2-, p38- or JNK-MAPK. Taken together, these data suggest that the long-term use of Empagliflozin in diabetic obese Zucker rats does not appear to affect the expression / activation of MAPK proteins in the EDL and soleus.

Subject(s)

Metabolic syndrome -- Research.

Metabolism -- Disorders -- Research.

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