Reversibility of the metabolic derangement and inflammation induced by nutritional obesity

2014 ◽  
Vol 233 (1) ◽  
pp. 330
Author(s):  
Maayan Vatarescu ◽  
Noa Slutsky ◽  
Tal Pecht ◽  
Ori Nov ◽  
Hagit Shapiro ◽  
...  
Animals ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 772
Author(s):  
Robert Ringseis ◽  
Denise K. Gessner ◽  
Frederik Loewenstein ◽  
Josef Kuehling ◽  
Sabrina Becker ◽  
...  

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.


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

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2643
Author(s):  
Rosa Cancelliere ◽  
Serena Leone ◽  
Cristina Gatto ◽  
Arianna Mazzoli ◽  
Carmine Ercole ◽  
...  

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.


Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Kamel A Gharaibeh ◽  
Vanessa Xanthakis ◽  
Jung Hye Sung ◽  
Tandaw S Samdarshi ◽  
Herman A Taylor ◽  
...  

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. -->


2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Michael A Burke ◽  
Stephen Chang ◽  
Danos C Christodoulou ◽  
Joshua M Gorham ◽  
Hiroko Wakimoto ◽  
...  

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.


2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Jai Sun Lee ◽  
Dae Won Jun ◽  
Eun Kyung Kim ◽  
Hye Joon Jeon ◽  
Ho Hyun Nam ◽  
...  

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.


2013 ◽  
Vol 46 (5) ◽  
pp. 307-312 ◽  
Author(s):  
Juliana Oggioni Gaiotti ◽  
Natália Delage Gomes ◽  
Ana Maria Doffémond Costa ◽  
Caroline Laurita Batista Couto Villela ◽  
Wanderval Moreira ◽  
...  

A literature review and pictorial essay were developed to discuss the importance of knowing the main findings and locations of otosclerosis at multidetector computed tomography (MDCT). The authors performed a retrospective review of cases of otosclerosis diagnosed in their institution by means of high resolution multidetector computed tomography. Otosclerosis corresponds to otic capsule dysplasia characterized by metabolic derangement of its endochondral layer. Such condition constitutes a relevant cause of sensorineural hearing loss, affecting about 7% to 10% of the general population. The diagnosis is usually clinical, but imaging methods play a significant role in the anatomical detailing, differential diagnosis, surgical planning and evaluation of postoperative complications. Among such methods, the relevance of MDCT is highlighted. Radiologists should be familiar with the MDCT findings of otosclerosis, as well as with the temporal bone anatomy to assist in the appropriate clinical management of this disease.


Author(s):  
Vivek Sharma ◽  
Sangeeta Bhattacharya ◽  
Poornima Dey Sarkar ◽  
Gini Garima ◽  
Neeraj Gour ◽  
...  

Background: Obesity is a complex disorder that involves some degree of over-consumption1 coupled with a metabolic derangement. As ADA has been putatively associated with inflammation, and adipose tissue inflammation is the hallmark of insulin resistance in obese T2DM patients. This study attempted to compare serum ADA in T2DM subjects.Methods: This observational cross-sectional study was conducted in the Department of Biochemistry at MGM Medical College and MY Hospital. All the patients and controls were clinically examined, and routine biochemical tests were analyzed for all subjects. ANOVA has been applied to assess the variance between groups.Results: Mean age of controls was 56.91 years where as mean age in the group of a subject with Obesity with diabetes was 40.91 years and with Obesity without diabetes was 48.10 years. ADA level was more among diabetes patients having obesity than diabetes patients having no obesity and controls.Conclusions: This is very much evident through this study that ADA may be treated as prognostic predictor of diabetes either linked to obesity or not, though more studies are warranted in same direction to make this finding conclusive and acceptable biochemical evidence.


2019 ◽  
Vol 19 (1) ◽  
pp. 37-41
Author(s):  
Salem A Beshyah ◽  
Brian M Frier

Diabetic ketoacidosis (DKA) is a life-threatening metabolic derangement, defined by the presence of severe hyperglycaemia, ketosis and metabolic acidosis. Recently, DKA was redefined to be present when the latter two abnormalities occur without severe hyperglycaemia. Munro and colleagues in Edinburgh described ‘euglycaemic diabetic ketoacidosis’ in 1973 and suggested this new terminology. The same year the critical feature of this subclass of DKA – that is, an increased urinary loss of glucose – was identified by Ireland and Thomson in Glasgow. In the subsequent 40 years (from 1974 to 2014), clinical interest in this condition was limited to a few case reports. The emergence of a new class of antidiabetes medications, the sodium-glucose cotransporter (SGLT) inhibitors, which promote profuse glycosuria, has reawakened interest in euglycaemic DKA, as this is a side effect of these drugs. The earlier perceptive observations of these physicians in Scotland deserve to be recognised for their contribution in identifying and describing euglycaemic DKA and correctly identifying its underlying pathogenesis. Recent international consensus has provided guidance to physicians to aid timely recognition of the condition by testing for ketosis in the appropriate clinical context and to manage it effectively by discontinuing the SGLT inhibitor and provision of insulin, carbohydrate and hydration (the STICH protocol). This may be particularly relevant in view of the recent licensing developments for use of certain members of the SGLT inhibitors in type 1 diabetes.


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