scholarly journals Obesity, metabolic derangement, and the risk of colorectal neoplasm

2021 ◽  
Vol 36 (7) ◽  
pp. 1731-1732
Author(s):  
Han‐Mo Chiu
Keyword(s):  
Colorectal Neoplasm ◽  
Metabolic Derangement

Analysis of age distribution of advanced colorectal neoplasm in average-risk Chinese

2013 ◽  
Vol 32 (4) ◽  
pp. 368-373
Author(s):  
Rong LIANG ◽  
En-da YU ◽  
Wei ZHU ◽  
Jie GAO ◽  
Zhao-shen LI ◽  
...  
Keyword(s):  
Colorectal Neoplasm ◽  
Age Distribution ◽  
Average Risk

Visceral obesity as a risk factor for colorectal neoplasm

2008 ◽  
Vol 23 (3) ◽  
pp. 411-417 ◽  
Author(s):  
Tae-Hoon Oh ◽  
Jeong-Sik Byeon ◽  
Seung-Jae Myung ◽  
Suk-Kyun Yang ◽  
Kwi-Sook Choi ◽  
...  
Keyword(s):  
Risk Factor ◽  
Colorectal Neoplasm ◽  
Visceral Obesity

scholarly journals Swine Inflammation and Necrosis Syndrome Is Associated with Plasma Metabolites and Liver Transcriptome in Affected Piglets

Animals ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 772
Author(s):  
Robert Ringseis ◽  
Denise K. Gessner ◽  
Frederik Loewenstein ◽  
Josef Kuehling ◽  
Sabrina Becker ◽  
...  
Keyword(s):  
Rna Splicing ◽  
Ribosome Biogenesis ◽  
Clinical Signs ◽  
Circulatory System ◽  
Plasma Metabolites ◽  
Biological Processes ◽  
High Group ◽  
Metabolic Derangement ◽  
Liver Transcriptome ◽  
Molecular Patterns

Swine Inflammation and Necrosis Syndrome can lead to severe clinical signs, especially in tails, ears, teats, and claws in pigs. Clinical and histopathological findings in newborn piglets with intact epidermis indicate a primarily endogenous etiology, and microbial-associated molecular patterns (MAMPs), such as lipopolysaccharide (LPS) are assumed to play a central role in the development of the syndrome. We hypothesized that swine inflammation and necrosis syndrome (SINS) is indirectly triggered by gut-derived MAMPs entering the circulatory system via the liver and thereby causing derangements on liver metabolism. To test this hypothesis, metabolomes, candidate genes of the liver and liver transcriptomes of 6 piglets with high-grade clinical signs of SINS (SINS high) were examined and compared with 6 piglets without significant signs of SINS (SINS low). Several hepatic pro-inflammatory genes and genes involved in stress response were induced in piglets of the SINS high group. The most striking finding from hepatic transcript profiling and bioinformatic enrichment was that the most enriched biological processes associated with the approximately 220 genes induced in the liver of the SINS high group were exclusively related to metabolic pathways, such as fatty acid metabolic process. Within the genes (≈390) repressed in the liver of the SINS high group, enriched pathways were ribosome biogenesis, RNA processing, RNA splicing, spliceosome, and RNA transport. The transcriptomic findings were supported by the results of the metabolome analyses. These results provide the first evidence for the induction of an inflammatory process in the liver of piglets suffering from SINS, accompanied by lipid metabolic derangement.

Hippo STK kinases drive metabolic derangement

2021 ◽  
Vol 3 (3) ◽  
pp. 295-296
Author(s):  
Kathrin Maedler ◽  
Amin Ardestani
Keyword(s):  
Metabolic Derangement

scholarly journals Metabolic Effects of the Sweet Protein MNEI as a Sweetener in Drinking Water. A Pilot Study of a High Fat Dietary Regimen in a Rodent Model

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2643
Author(s):  
Rosa Cancelliere ◽  
Serena Leone ◽  
Cristina Gatto ◽  
Arianna Mazzoli ◽  
Carmine Ercole ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Profile ◽  
Western Diet ◽  
Metabolic Effects ◽  
High Fat ◽  
Metabolic Derangement ◽  
Dietary Regimen ◽  
Sweet Proteins ◽  
Sweet Protein ◽  
Typical Western Diet

Sweeteners have become integrating components of the typical western diet, in response to the spreading of sugar-related pathologies (diabetes, obesity and metabolic syndrome) that have stemmed from the adoption of unbalanced dietary habits. Sweet proteins are a relatively unstudied class of sweet compounds that could serve as innovative sweeteners, but their introduction on the food market has been delayed by some factors, among which is the lack of thorough metabolic and toxicological studies. We have tried to shed light on the potential of a sweet protein, MNEI, as a fructose substitute in beverages in a typical western diet, by studying the metabolic consequences of its consumption on a Wistar rat model of high fat diet-induced obesity. In particular, we investigated the lipid profile, insulin sensitivity and other indicators of metabolic syndrome. We also evaluated systemic inflammation and potential colon damage. MNEI consumption rescued the metabolic derangement elicited by the intake of fructose, namely insulin resistance, altered plasma lipid profile, colon inflammation and translocation of lipopolysaccharides from the gut lumen into the circulatory system. We concluded that MNEI could represent a valid alternative to fructose, particularly when concomitant metabolic disorders such as diabetes and/or glucose intolerance are present.

scholarly journals Mapping the Functional Assessment of Cancer Therapy-General or -Colorectal to SF-6D in Chinese Patients with Colorectal Neoplasm

2012 ◽  
Vol 15 (3) ◽  
pp. 495-503 ◽  
Author(s):  
Carlos K.H. Wong ◽  
Cindy L.K. Lam ◽  
Donna Rowen ◽  
Sarah M. McGhee ◽  
Ka-Ping Ma ◽  
...  
Keyword(s):  
Cancer Therapy ◽  
Functional Assessment ◽  
Colorectal Neoplasm ◽  
Chinese Patients

Abstract P439: Risk Factor Profile and Prevalence of Subclinical Disease in African Americans with Diabetes and Metabolic Syndrome: The Jackson Heart Study

Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Kamel A Gharaibeh ◽  
Vanessa Xanthakis ◽  
Jung Hye Sung ◽  
Tandaw S Samdarshi ◽  
Herman A Taylor ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Risk Factor ◽  
African Americans ◽  
Left Ventricular ◽  
Jackson Heart Study ◽  
Cvd Risk ◽  
Metabolic Derangement ◽  
Risk Factor Profile ◽  
Subclinical Disease ◽  
Heart Study

Background . Metabolic derangements such as diabetes (DM) and metabolic syndrome (MetS) are common in African Americans (AA) and contribute to the higher cardiovascular disease (CVD) mortality in this group. A greater prevalence of subclinical disease (ScD) among those with DM and MetS in the AA community may be an explanatory factor. Objective . We assessed the CVD risk factor profile and distribution of ScD among AA with DM and MetS in the Jackson Heart Study (JHS). Methods . We evaluated 4,365 AA participants [mean age (SD) of 53.8 (12.3) years, 64.5% women] free of overt CVD who attended JHS Exam 1 (between 2000- 2004), when ScD assessment was routinely performed(with the exception of CT for coronary calcium that occurred in Exam2). SCD measures included 1) peripheral artery disease (PAD, defined as ankle-brachial index<0.9), 2) high coronary artery calcium (CAC, defined as score>100), 3) left ventricular (LV) hypertrophy (LVH defined as left ventricular mass index>51 g/m 2.7 , 4) low LV ejection fraction (low EF, defined as an EF<50%), and 5) microalbuminuria (MA, defined as an albumin-to-creatinine ratio>25 μg/mg in men and >35 μg/mg in women). We compared the distribution of standard CVD risk factors and ScD prevalence in 1) those without DM or MetS (referent), 2) those with MetS but no DM and 3) those with DM. Results . In our study sample, 1,089 (24.9%) had MetS with no DM and 752 (17.2%) had DM. Compared to the referent group, groups with metabolic derangement tended to be older, female, hypertensive, obese, and had lower HDL, higher fasting glucose, and higher triglycerides levels. Table 1 compares the distribution of ScD for the three groups, and demonstrates the greater odds of. CAC, LVH and microalbuminuria in participants with MetS or DM. Conclusion . In our large community-based sample of AAs, we observed a significantly high prevalence of ScD overall, especially so in participants with MetS and DM. These findings likely contribute to the high CVD rates in AA with MetS and DM. -->

Abstract 290: Proliferation of Cardiac Fibroblasts Defines Early Stages of Genetic Dilated Cardiomyopathy and Precedes Myocardial Metabolic Derangement

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Michael A Burke ◽  
Stephen Chang ◽  
Danos C Christodoulou ◽  
Joshua M Gorham ◽  
Hiroko Wakimoto ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cardiac Fibroblasts ◽  
Expression Patterns ◽  
Molecular Networks ◽  
Peroxisome Proliferator ◽  
Metabolic Derangement ◽  
Peroxisome Proliferator Activated Receptor ◽  
Cell Remodeling ◽  
Ppar Signaling ◽  
Myocyte Proliferation

The complex molecular networks underpinning DCM remain poorly understood. To study distinct pathways and networks in the longitudinal development of DCM we performed RNAseq on LV tissue from mice carrying a human DCM mutation in phospholamban (PLN R9C/+ ) before phenotype onset (pre-DCM), with DCM, and during overt heart failure (HF), and also on isolated myocytes and non-myocytes from DCM hearts. PLN R9C/+ mice show progressive fibrosis (20% vs. 1% control, p=6x10 −33 ; n=3) associated with proliferation of cardiac non-myocytes (33% increase over control, p=6x10 −4 ; n=3). Consistent with this, cardiac non-myocytes have upregulated gene expression and pathways, while these are generally downregulated in myocytes. Non-myocytes were enriched in fibrosis, inflammation, and cell remodeling pathways, from pre-DCM to HF. In contrast, myocytes were enriched for metabolic pathways only with overt DCM and HF. Myocytes showed profound derangement of oxidative phosphorylation with DCM (p=2.5x10 −41 ; 44% (53/120) of pathway genes downregulated), suggesting mitochondrial dysfunction. Additionally, we detected probable inhibition of peroxisome proliferator-activated receptor (PPAR) signaling by diminished expression of pathway genes (Figure). DCM and hypertrophic remodeling was compared using RNAseq of a mouse model of HCM; similar patterns of fibrosis with myocyte metabolic dysregulation were evident despite unique differential gene expression patterns between models. DCM caused by PLN R9C/+ is associated with early non-myocyte proliferation and later myocyte metabolic derangement possibly governed by altered PPAR signaling, and is common to DCM and HCM.

scholarly journals Histologic and Metabolic Derangement in High-Fat, High-Fructose, and Combination Diet Animal Models

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Jai Sun Lee ◽  
Dae Won Jun ◽  
Eun Kyung Kim ◽  
Hye Joon Jeon ◽  
Ho Hyun Nam ◽  
...  
Keyword(s):  
Animal Model ◽  
Body Weight Gain ◽  
Tolerance Test ◽  
Combination Group ◽  
Oral Glucose ◽  
High Fat ◽  
Metabolic Derangement ◽  
Fat Accumulation ◽  
Nonalcoholic Fatty Liver ◽  
High Fructose

Background. We used high-fat (HF), high-fructose (HFr), and combination diets to create a dietary animal model of nonalcoholic fatty liver disease (NAFLD). Comparison of both clinical phenotypes has not been well defined. The purpose of this study was to compare histologic and metabolic characteristics between diets in an animal model of NAFLD.Methods. NAFLD was induced in rats by feeding them HF, HFr, and combination (HF + HFr) diets for 20 weeks. The degree of intrahepatic fat accumulation, inflammation, and oxidative stress was evaluated. Metabolic derangements were assessed by the oral glucose tolerance test and the intrahepatic insulin signal pathway.Results. Body weight gain and intrahepatic fat accumulation were more prominent in the HF feeding group than in the HFr group. The expressions of NOX-4 and TLR-4 were higher in the HF and HFr combination groups than in the HF-only group. Other intrahepatic inflammatory markers, MCP-1, TNF-α, and endoplasmic reticulum stress markers, were the highest in the HF + HFr combination group. Although intrahepatic fat deposition was less prominent in the HFr diet model, intrahepatic inflammation was noted.Conclusions. Intrahepatic inflammation and metabolic derangements were more prominent in the HF and HFr combination model than in the HF monodiet model.

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