Browsing by Author "Kim, Jung Han"
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Item Tart cherry reduces inflammation in adipose tissue of zucker fatty rats and cultured 3T3-L1 adipocytes(2018) Jayarathne, Shasika (TTU); Stull, April J.; Miranda, Alexandra (TTU); Scoggin, Shane (TTU); Claycombe-Larson, Kate; Kim, Jung Han; Moustaid-Moussa, Naima (TTU)Obesity increases adipose tissue inflammation and secretion of pro-inflammatory adipokines, which have systemic effects on the organism’s health status. Our objective was to dissect mechanisms of anti-inflammatory effects of tart cherry (TC) in adipose tissue of Zucker fatty rats, and cultured 3T3-L1 adipocytes. Rats were fed either a control diet, or 4% TC powder diets for eight weeks. Body and epididymal fat pad weights were not significantly different between control and TC groups. However, rats fed the TC diet had significantly reduced adipose tissue inflammation (p < 0.05), as determined by reduced mRNA levels of pro-inflammatory markers including interleukin-6 (IL-6), tumor necrosis factor alpha (TNFα), interleukin-1beta (IL-1β), monocyte chemoattractant protein 1 (MCP-1), inducible nitric oxide synthase (iNOS), and CD-11b, and increased mRNA levels of type-1 arginase (Arg-1) anti-inflammatory marker. Consistent with these in vivo results, TC significantly decreased expression of IL-6 mRNA and protein levels in lipopolysaccharide (LPS) stimulated adipocytes compared to those stimulated with LPS, but no TC. Moreover, both in vivo (rat adipose tissue) and in vitro (3T3-L1 adipocytes), phosphorylation of p65-NF-κB subunit was significantly reduced by TC. Additionally, TC decreased mRNA expression of fatty acid synthase (FASN), and increased expression of peroxisome proliferator-activated receptor alpha (PPARα), master regulator of lipid oxidation, and anti-oxidant markers nuclear factor erythroid-derived 2-related factor (NRFs) in both models. In conclusion, our findings indicate that TC downregulates inflammation in part via the nuclear factor kappa B (NF-κB) pathway in adipose tissue. Thus, TC may serve as a potential intervention to reduce obesity-associated inflammation.Item Transgenic mice overexpressing renin exhibit glucose intolerance and diet-genotype interactions(2013) Fletcher, Sarah J.; Kalupahana, Nishan S.; Soltani-Bejnood, Morvarid; Kim, Jung Han; Saxton, Arnold M.; Wasserman, David H.; De Taeye, Bart; Voy, Brynn H.; Quignard-Boulange, Annie; Moustaid-Moussa, Naima (TTU)Numerous animal and clinical investigations have pointed to a potential role of the renir angiotensin system (RAS) in the development of insulin resistance and diabetes in cond tions of expanded fat mass. However, the mechanisms underlying this association remai unclear. We used a transgenic mouse model overexpressing renin in the liver (RenTgMK) to examine the effects of chronic activation of RAS on adiposity and insulin sensitivity. Hepatic overexpression of renin resulted in constitutively elevated plasma angiotensin (four- to six-fold increase vs. wild-type, WT). Surprisingly, RenTgMK mice developed gl cose intolerance despite low levels of adiposity and insulinemia. The transgenics also had lower plasma triglyceride levels. Glucose intolerance in transgenic mice fed a low-fat die was comparable to that observed in high-fat fed WT mice. These studies demonstrate that overexpression of renin and associated hyperangiotensinemia impair glucose tolerance i a diet-dependent manner and further support a consistent role of RAS in the pathogenesi of diabetes and insulin resistance, independent of changes in fat mass. © 2013 Fletcher, Kalupahana, Soltani-Bejnood, Kim, Saxton, Wasser-man, DeTaeye, Voy, Quignard-Boulange and Moustaid-Moussa.