Browsing by Author "Zhou, Jing"

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    Effects of a High-Protein Diet Including Whole Eggs on Muscle Composition and Indices of Cardiometabolic Health and Systemic Inflammation in Older Adults with Overweight or Obesity: A Randomized Controlled Trial
    (MDPI, 2018-07-23) Wright, Christian S.; Zhou, Jing; Sayer, R. Drew; Kim, Jung Eun; Campbell, Wayne W.; Physical Therapy, School of Health and Human Sciences
    Age-related increases in intermuscular adipose tissue (IMAT) impair muscle quality, decrease functional capacity, and promote several cardiometabolic and inflammatory disorders. Whether these age-related alterations in muscle composition improve by consuming a high-protein (HP) diet with whole eggs are unclear. This parallel-design, randomized-controlled trial assessed the effects of a 12-week eucaloric HP diet with three whole eggs per day (1.4 g protein kg-1 day-1) versus a normal-protein diet void of eggs (NP, 0.8 g protein kg-1 day-1) on muscle composition (IMAT), cardiometabolic health, and systemic inflammation in older adults with overweight or obesity (12 men and 10 women; age 70 ± 5 years, BMI 31.3 ± 3.2 kg/m², mean ± SD). No changes in muscle composition were observed over time, independent of protein intake. Total body weight was reduced in both groups (-3.3 ± 1.2%) and lean mass was preserved only with the HP diet. LDL concentration and hip circumference decreased only with the NP diet, while MCP-1 and HsCRP concentrations increased over time in both groups. A HP diet with whole eggs promotes lean mass retention with modest weight loss, but does not positively influence muscle composition, cardiometabolic health or systemic inflammation, compared to a NP diet void of eggs.
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    Indole Alleviates Diet-induced Hepatic Steatosis and Inflammation in a Manner Involving Myeloid Cell PFKFB3
    (Wolters Kluwer, 2020-10) Ma, Linqiang; Li, Honggui; Hu, Jinbo; Zheng, Juan; Zhou, Jing; Botchlett, Rachel; Matthews, Destiny; Zeng, Tianshu; Chen, Lulu; Xiao, Xiaoqiu; Athrey, Giri; Threadgill, David W.; Li, Qingsheng; Glaser, Shannon; Francis, Heather; Meng, Fanyin; Li, Qifu; Alpini, Gianfranco; Wu, Chaodong; Medicine, School of Medicine
    Background and aims: Indole is a microbiota metabolite that exerts anti-inflammatory responses. However, the relevance of indole to human non-alcoholic fatty liver disease (NAFLD) is not clear. It also remains largely unknown whether and how indole acts to protect against NAFLD. The present study sought to examine the association between the circulating levels of indole and liver fat content in human subjects and explore the mechanisms underlying indole actions in mice with diet-induced NAFLD. Approach and results: In a cohort of 137 subjects, the circulating levels of indole were reversely correlated with body mass index. In addition, the circulating levels of indole in obese subjects were significantly lower than those in lean subjects and were accompanied with increased liver fat content. At the whole-animal level, treatment of high-fat diet (HFD)-fed C57BL/6J mice with indole caused significant decreases in the severity of hepatic steatosis and inflammation. In cultured cells, indole treatment stimulated the expression of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), a master regulatory gene of glycolysis, and suppressed macrophage proinflammatory activation in a PFKFB3-dependent manner. Moreover, myeloid cell-specific PFKFB3 disruption exacerbated the severity of HFD-induced hepatic steatosis and inflammation and blunted the effect of indole on alleviating diet-induced NAFLD phenotype. Conclusions: Taken together, our results demonstrate that indole is relevant to human NAFLD and capable of alleviating diet-induced NAFLD phenotypes in mice in a myeloid cell PFKFB3-dependent manner. Therefore, indole mimetic and/or macrophage-specific PFKFB3 activation may be the viable preventive and/or therapeutic approaches for inflammation-associated diseases including NAFLD.
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    An integrated investigation of lake storage and water level changes in the Paiku Co basin, central Himalayas
    (Elsevier, 2018) Lei, Yanbin; Yao, Tandong; Yang, Kun; Bird, Broxton W.; Tian, Lide; Zhang, Xiaowen; Wang, Weicai; Xiang, Yang; Dai, Yufeng; Lazhu; Zhou, Jing; Wang, Lei; Earth Sciences, School of Science
    Since the late 1990s, lakes in the southern Tibetan Plateau (TP) have shrunk considerably, which contrasts with the rapid expansion of lakes in the interior TP. Although these spatial trends have been well documented, the underlying hydroclimatic mechanisms are not well understood. Since 2013, we have carried out comprehensive water budget observations at Paiku Co, an alpine lake in the central Himalayas. In this study, we investigate water storage and lake level changes on seasonal to decadal time scales based on extensive in-situ measurements and satellite observations. Bathymetric surveys show that Paiku Co has a mean and maximum water depth of 41.1 m and 72.8 m, respectively, and its water storage was estimated to be 109.3 × 108 m3 in June 2016. On seasonal scale between 2013 and 2017, Paiku Co’s lake level decreased slowly between January and May, increased considerably between June and September, and then decreased rapidly between October and January. On decadal time scale, Paiku Co’s lake level decreased by 3.7 ± 0.3 m and water storage reduced by (10.2 ± 0.8) × 108 m3 between 1972 and 2015, accounting for 8.5% of the total water storage in 1972. This change is consistent with a trend towards drier conditions in the Himalaya region during the recent decades. In contrast, glacial lakes within Paiku Co’s basin expanded rapidly, indicating that, unlike Paiku Co, glacial meltwater was sufficient to compensate the effect of the reduced precipitation.
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    Methionine- and Choline-Deficient Diet-Induced Nonalcoholic Steatohepatitis Is Associated with Increased Intestinal Inflammation
    (Elsevier, 2021) Matthews, Destiny R.; Li, Honggui; Zhou, Jing; Li, Qingsheng; Glaser, Shannon; Francis, Heather; Alpini, Gianfranco; Wu, Chaodong; Medicine, School of Medicine
    Inflammation drives the pathogenesis of nonalcoholic steatohepatitis (NASH). The current study examined changes in intestinal inflammation during NASH. In male C57BL/6J mice, feeding a methionine- and choline-deficient diet (MCD) resulted in severe hepatic steatosis and inflammation relative to feeding a chow diet (CD). MCD-fed mice exhibited characteristics of mucosal and submucosal inflammatory responses compared with CD-fed mice. Moreover, intestinal phosphorylation states of c-Jun N-terminal protein kinase p46 and mRNA levels of IL-1B, IL-6, tumor necrosis factor alpha, and monocyte chemoattractant protein-1 were significantly higher and intestinal mRNA levels of IL-4 and IL-13 were significantly lower in MCD-fed mice compared with those in CD mice. Surprisingly, upon treatment with MCD-mimicking media, the proinflammatory responses in cultured intestinal epithelial CMT-93 cells did not differ significantly from those in CMT-93 cells treated with control media. In contrast, in RAW264.7 macrophages, MCD-mimicking media significantly increased the phosphorylation states of c-Jun N-terminal protein kinase p46 and mitogen-activated protein kinases p38 and mRNA levels of IL-1B, IL-6, IL-10, and tumor necrosis factor alpha under either basal or lipopolysaccharide-stimulated conditions. Collectively, these results suggest that increased intestinal inflammation is associated with NASH phenotype. Thus, elevated proinflammatory responses in macrophages likely contribute to, in large part, increased intestinal inflammation in NASH.
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    Survivin-induced abnormal ploidy contributes to cystic kidney and aneurysm formation
    (Ovid Technologies Wolters Kluwer -American Heart Association, 2014-02-11) AbouAlaiwi, Wissam A.; Muntean, Brian S.; Ratnam, Shobha; Joe, Bina; Liu, Lijun; Booth, Robert L.; Rodriguez, Ingrid; Herbert, Britney S.; Bacallao, Robert L.; Fruttiger, Marcus; Mak, Tak W.; Zhou, Jing; Nauli, Surya M.; Department of Medical and Molecular Genetics, IU School of Medicine
    BACKGROUND: Cystic kidneys and vascular aneurysms are clinical manifestations seen in patients with polycystic kidney disease, a cilia-associated pathology (ciliopathy). Survivin overexpression is associated with cancer, but the clinical pathology associated with survivin downregulation or knockout has never been studied before. The present studies aim to examine whether and how cilia function (Pkd1 or Pkd2) and structure (Tg737) play a role in cystic kidney and aneurysm through survivin downregulation. METHODS AND RESULTS: Cysts and aneurysms from polycystic kidney disease patients, Pkd mouse, and zebrafish models are characterized by chromosome instability and low survivin expression. This triggers cytokinesis defects and formation of nuclear polyploidy or aneuploidy. In vivo conditional mouse and zebrafish models confirm that survivin gene deletion in the kidneys results in a cystic phenotype. As in hypertensive Pkd1, Pkd2, and Tg737 models, aneurysm formation can also be induced in vascular-specific normotensive survivin mice. Survivin knockout also contributes to abnormal oriented cell division in both kidney and vasculature. Furthermore, survivin expression and ciliary localization are regulated by flow-induced cilia activation through protein kinase C, Akt and nuclear factor-κB. Circumventing ciliary function by re-expressing survivin can rescue polycystic kidney disease phenotypes. CONCLUSIONS: For the first time, our studies offer a unifying mechanism that explains both renal and vascular phenotypes in polycystic kidney disease. Although primary cilia dysfunction accounts for aneurysm formation and hypertension, hypertension itself does not cause aneurysm. Furthermore, aneurysm formation and cyst formation share a common cellular and molecular pathway involving cilia function or structure, survivin expression, cytokinesis, cell ploidy, symmetrical cell division, and tissue architecture orientation.
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    A translational bioinformatic approach in identifying and validating an interaction between Vitamin A and CYP19A1
    (Springer (Biomed Central Ltd.), 2015) Philips, Santosh; Zhou, Jing; Li, Zhigao; Skaar, Todd C.; Li, Lang; Department of Medicine, IU School of Medicine
    INTRODUCTION: One major challenge in personalized medicine research is to identify the environmental factors that can alter drug response, and to investigate their molecular mechanisms. These environmental factors include co-medications, food, and nutrition or dietary supplements. The increasing use of dietary supplements and their potential interactions with cytochrome P450 (CYP450) enzymes is a highly significant personalized medicine research domain, because most of the drugs on the market are metabolized through CYP450 enzymes. METHODS: Initial bioinformatics analysis revealed a number of regulators of CYP450 enzymes from a human liver bank gene expression quantitative loci data set. Then, a compound-gene network was constructed from the curated literature data. This network consisted of compounds that interact with either CYPs and/or their regulators that influence either their gene expression or activity. We further evaluated this finding in three different cell lines: JEG3, HeLa, and LNCaP cells. RESULTS: From a total of 868 interactions we were able to identify an interesting interaction between retinoic acid (i.e. Vitamin A) and the aromatase gene (i.e. CYP19A1). Our experimental results showed that retinoic acid at physiological concentration significantly influenced CYP19A1 gene expressions. CONCLUSIONS: These results suggest that the presence of retinoic acid may alter the efficacy of agents used to suppress aromatase expression.
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    Weight loss achieved using an energy restriction diet with normal or higher dietary protein decreased the number of CD14++CD16+ proinflammatory monocytes and plasma lipids and lipoproteins in middle-aged, overweight, and obese adults
    (Elsevier, 2017-04) Kim, Jung Eun; Lin, Ge; Zhou, Jing; Mund, Julie Ann; Case, Jamie; Campbell, Wayne W.; Department of Pediatrics, IU School of Medicine
    Monocytes are involved in immune responses, and specific monocyte subpopulations (MS) that express intermediate to high levels of CD16 are associated with obesity and cardiovascular events. Consuming high protein (HP) when dieting improves body composition and cardiometabolic health outcomes, but whether HP affects MS during weight loss remains unknown. We assessed the effect of HP on energy restriction (ER)–induced changes in MS in overweight and obese adults. The relations between MS and plasma lipids and lipoproteins were also examined. We hypothesized that, independent of protein intake, ER-induced weight loss would decrease the numbers of MS and that MS and plasma lipids and lipoproteins would be related. Thirty-two adults (age 52 ± 1 years, body mass index 31.3 ± 0.5 kg/m2, means ± S.E.) consumed either a normal protein (n=18) or HP (n=14) (0.8 vs 1.5 g•kg−1•d−1 protein) ER diet (750-kcal/d [3138-kJ/d] deficit) for 16 weeks. The HP diet included 0.7 g•kg−1•d−1 of milk protein isolate. Fasting plasma lipids, lipoproteins, and the numbers of MS were analyzed. Over time, independent of protein intake, CD14++CD16+ cell number decreased, whereas CD14dimCD16++, CD14+CD16+, and CD14+CD16− cell numbers remained unchanged. CD14dimCD16++ cell number was negatively associated with total cholesterol (TC) and triglyceride, while CD14++CD16+ cell number was positively associated with TC, low-density lipoprotein cholesterol (LDL), TC to high-density lipoprotein cholesterol (HDL) ratio, and LDL to HDL ratio. Weight loss achieved while consuming an ER diet with either normal or high protein may improve immunity by partially decreasing proinflammatory monocytes. Associations between MS and plasma lipids and lipoproteins are confirmed in overweight and obese adults.