scholarly journals Mechanisms Mediating Anti-Inflammatory Effects of Delta-Tocotrienol and Tart Cherry Anthocyanins in 3T3-L1 Adipocytes

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3356
Author(s):  
Lexie Harlan ◽  
London T. Mena ◽  
Latha Ramalingam ◽  
Shasika Jayarathne ◽  
Chwan-Li Shen ◽  
...  
Keyword(s):  
Metabolic Diseases ◽  
Combined Treatment ◽  
Low Grade ◽  
Tart Cherry ◽  
Metabolic Complications ◽  
Inflammatory Protein ◽  
Anti Inflammatory ◽  
Low Grade Inflammation ◽  
Macrophage Inflammatory Protein

Chronic low-grade inflammation is a primary characteristic of obesity and can lead to other metabolic complications including insulin resistance and type 2 diabetes (T2D). Several anti-inflammatory dietary bioactives decrease inflammation that accompanies metabolic diseases. We are specifically interested in delta-tocotrienol, (DT3) an isomer of vitamin E, and tart cherry anthocyanins (TCA), both of which possess individual anti-inflammatory properties. We have previously demonstrated that DT3 and TCA, individually, reduced systemic and adipose tissue inflammation in rodent models of obesity. However, whether these compounds have combinatorial effects has not been determined yet. Hence, we hypothesize that a combined treatment of DT3 and TCA will have great effects in reducing inflammation in adipocytes, and that these effects are mediated via the nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB), a major inflammatory transcription factor. We used 3T3-L1 adipocytes and treated them with 1–5 µM doses of DT3 along with tart cherry containing 18–36 µg anthocyanin/mL, to assess effects on inflammation. Neither DT3 nor TCA, nor their combinations had toxic effects on adipocytes. Furthermore, pro-inflammatory markers interleukin-6 (IL-6) and p-65 (subunit of NFkB) were reduced at the protein level in media collected from adipocytes with both individual and combined treatments. Additionally, other downstream targets of NFkB including macrophage inflammatory protein 2 (Mip2), and Cyclooxygenase-2 (Cox2) were also significantly downregulated (p ≤ 0.05) when treated with individual and combined doses of DT3 and TCA with no additional combinatorial effects. In summary, DT3 and TCA individually, are beneficial in reducing inflammation with no additional combinatorial effects.

scholarly journals Amelioration of metabolic syndrome by metformin associates with reduced indices of low-grade inflammation independently of the gut microbiota

2019 ◽  
Vol 317 (6) ◽  
pp. E1121-E1130 ◽  
Author(s):  
Aneseh Adeshirlarijaney ◽  
Jun Zou ◽  
Hao Q. Tran ◽  
Benoit Chassaing ◽  
Andrew T. Gewirtz
Keyword(s):  
Metabolic Syndrome ◽  
Gut Microbiota ◽  
Early Stage ◽  
Mechanisms Of Action ◽  
Low Grade ◽  
Inflammatory Agent ◽  
Frontline Treatment ◽  
Anti Inflammatory ◽  
Low Grade Inflammation

Metformin beneficially impacts several aspects of metabolic syndrome including dysglycemia, obesity, and liver dysfunction, thus making it a widely used frontline treatment for early-stage type 2 diabetes, which is associated with these disorders. Several mechanisms of action for metformin have been proposed, including that it acts as an anti-inflammatory agent, possibly as a result of its impact on intestinal microbiota. In accord with this possibility, we observed herein that, in mice with diet-induced metabolic syndrome, metformin impacts the gut microbiota by preventing its encroachment upon the host, a feature of metabolic syndrome in mice and humans. However, the ability of metformin to beneficially impact metabolic syndrome in mice was not markedly altered by reduction or elimination of gut microbiota, achieved by the use of antibiotics or germfree mice. Although reducing or eliminating microbiota by itself suppressed diet-induced dysglycemia, other features of metabolic syndrome including obesity, hepatic steatosis, and low-grade inflammation remained suppressed by metformin in the presence or absence of gut microbiota. These results support a role for anti-inflammatory activity of metformin, irrespective of gut microbiota, in driving some of the beneficial impacts of this drug on metabolic syndrome.

Lifestyle Measures to Reduce Inflammation

2011 ◽  
Vol 6 (1) ◽  
pp. 4-13 ◽  
Author(s):  
Glenn A. Gaesser ◽  
Siddhartha S. Angadi ◽  
Dana M. Ryan ◽  
Carol S. Johnston
Keyword(s):  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Aerobic Exercise ◽  
Inflammatory Markers ◽  
Dietary Factors ◽  
Low Grade ◽  
Inflammatory Status ◽  
Anti Inflammatory ◽  
Low Grade Inflammation

Chronic low-grade inflammation associated with cardiovascular disease and type 2 diabetes (T2D) may be ameliorated with exercise and/or diet. High levels of physical activity and/or cardiorespiratory fitness are associated with reduced risk of low-grade inflammation. Both aerobic and resistance exercise have been found to improve inflammatory status, with the majority of evidence suggesting that aerobic exercise may have broader anti-inflammatory effects. In particular, aerobic exercise appears to improve the balance between pro- and anti-inflammatory markers. Improvement in inflammatory status is most likely to occur in persons with elevated levels of pro-inflammatory markers prior to intervention. A number of dietary factors, including fiber-rich foods, whole grains, fruits (especially berries), omega-3 fatty acids, antioxidant vitamins (eg, C and E), and certain trace minerals (eg, zinc) have been documented to reduce blood concentrations of inflammatory markers. Anti-inflammatory foods may also help mitigate the pro-inflammatory postprandial state that is particularly evident after ingestion of meals high in saturated fat. Intensive lifestyle interventions involving both exercise and diet appear to be most effective. For the most part, anti-inflammatory effects of exercise and diet are independent of weight loss. Thus overweight and obese men and women, who are most likely to have a pro-inflammatory profile, do not necessarily have to normalize body mass index to improve inflammatory status and reduce risk of type 2 diabetes and cardiovascular disease.

scholarly journals Berries as a Treatment for Obesity-Induced Inflammation: Evidence from Preclinical Models

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 334
Author(s):  
Hannah Land Lail ◽  
Rafaela G. Feresin ◽  
Dominique Hicks ◽  
Blakely Stone ◽  
Emily Price ◽  
...  
Keyword(s):  
Chronic Diseases ◽  
Low Grade ◽  
Bioactive Components ◽  
Preclinical Models ◽  
Beneficial Effects ◽  
Increased Risk ◽  
Anti Inflammatory ◽  
Treatment Of Obesity ◽  
Low Grade Inflammation

Inflammation that accompanies obesity is associated with the infiltration of metabolically active tissues by inflammatory immune cells. This propagates a chronic low-grade inflammation associated with increased signaling of common inflammatory pathways such as NF-κB and Toll-like receptor 4 (TLR4). Obesity-associated inflammation is linked to an increased risk of chronic diseases, including type 2 diabetes, cardiovascular disease, and cancer. Preclinical rodent and cell culture studies provide robust evidence that berries and their bioactive components have beneficial effects not only on inflammation, but also on biomarkers of many of these chronic diseases. Berries contain an abundance of bioactive compounds that have been shown to inhibit inflammation and to reduce reactive oxygen species. Therefore, berries represent an intriguing possibility for the treatment of obesity-induced inflammation and associated comorbidities. This review summarizes the anti-inflammatory properties of blackberries, blueberries, strawberries, and raspberries. This review highlights the anti-inflammatory mechanisms of berries and their bioactive components that have been elucidated through the use of preclinical models. The primary mechanisms mediating the anti-inflammatory effects of berries include a reduction in NF-κB signaling that may be secondary to reduced oxidative stress, a down-regulation of TLR4 signaling, and an increase in Nrf2.

scholarly journals Activation of the nuclear factor-κB pathway during postnatal lung inflammation preserves alveolarization by suppressing macrophage inflammatory protein-2

2015 ◽  
Vol 309 (6) ◽  
pp. L593-L604 ◽  
Author(s):  
Yanli Hou ◽  
Min Liu ◽  
Cristiana Husted ◽  
Chihhsin Chen ◽  
Kavitha Thiagarajan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Combined Treatment ◽  
Nuclear Factor Κb ◽  
Inflammatory Stress ◽  
Inflammatory Protein ◽  
Inflammatory Stimuli ◽  
Anti Inflammatory ◽  
Macrophage Inflammatory Protein

A significant portion of lung development is completed postnatally during alveolarization, rendering the immature lung vulnerable to inflammatory stimuli that can disrupt lung structure and function. Although the NF-κB pathway has well-recognized pro-inflammatory functions, novel anti-inflammatory and developmental roles for NF-κB have recently been described. Thus, to determine how NF-κB modulates alveolarization during inflammation, we exposed postnatal day 6 mice to vehicle (PBS), systemic lipopolysaccharide (LPS), or the combination of LPS and the global NF-κB pathway inhibitor BAY 11-7082 (LPS + BAY). LPS impaired alveolarization, decreased lung cell proliferation, and reduced epithelial growth factor expression. BAY exaggerated these detrimental effects of LPS, further suppressing proliferation and disrupting pulmonary angiogenesis, an essential component of alveolarization. The more severe pathology induced by LPS + BAY was associated with marked increases in lung and plasma levels of macrophage inflammatory protein-2 (MIP-2). Experiments using primary neonatal pulmonary endothelial cells (PEC) demonstrated that MIP-2 directly impaired neonatal PEC migration in vitro; and neutralization of MIP-2 in vivo preserved lung cell proliferation and pulmonary angiogenesis and prevented the more severe alveolar disruption induced by the combined treatment of LPS + BAY. Taken together, these studies demonstrate a key anti-inflammatory function of the NF-κB pathway in the early alveolar lung that functions to mitigate the detrimental effects of inflammation on pulmonary angiogenesis and alveolarization. Furthermore, these data suggest that neutralization of MIP-2 may represent a novel therapeutic target that could be beneficial in preserving lung growth in premature infants exposed to inflammatory stress.

scholarly journals The anti-inflammatory function of HDL is impaired in type 2 diabetes: role of hyperglycemia, paraoxonase-1 and low grade inflammation

2017 ◽  
Vol 16 (1) ◽  
Author(s):  
Sanam Ebtehaj ◽  
Eke G. Gruppen ◽  
Mojtaba Parvizi ◽  
Uwe J. F. Tietge ◽  
Robin P. F. Dullaart
Keyword(s):  
Type 2 Diabetes ◽  
Paraoxonase 1 ◽  
Low Grade ◽  
Anti Inflammatory ◽  
Low Grade Inflammation

scholarly journals Association of Adipose Tissue and Adipokines with Development of Obesity-Induced Liver Cancer

2021 ◽  
Vol 22 (4) ◽  
pp. 2163
Author(s):  
Yetirajam Rajesh ◽  
Devanand Sarkar
Keyword(s):  
Adipose Tissue ◽  
Cancer Progression ◽  
Metabolic Diseases ◽  
Low Grade ◽  
Metabolic Complications ◽  
Endocrine Organ ◽  
Nonalcoholic Fatty Liver ◽  
Underlying Mechanisms ◽  
Low Grade Inflammation ◽  
Excessive Accumulation

Obesity is rapidly dispersing all around the world and is closely associated with a high risk of metabolic diseases such as insulin resistance, dyslipidemia, and nonalcoholic fatty liver disease (NAFLD), leading to carcinogenesis, especially hepatocellular carcinoma (HCC). It results from an imbalance between food intake and energy expenditure, leading to an excessive accumulation of adipose tissue (AT). Adipocytes play a substantial role in the tumor microenvironment through the secretion of several adipokines, affecting cancer progression, metastasis, and chemoresistance via diverse signaling pathways. AT is considered an endocrine organ owing to its ability to secrete adipokines, such as leptin, adiponectin, resistin, and a plethora of inflammatory cytokines, which modulate insulin sensitivity and trigger chronic low-grade inflammation in different organs. Even though the precise mechanisms are still unfolding, it is now established that the dysregulated secretion of adipokines by AT contributes to the development of obesity-related metabolic disorders. This review focuses on several obesity-associated adipokines and their impact on obesity-related metabolic diseases, subsequent metabolic complications, and progression to HCC, as well as their role as potential therapeutic targets. The field is rapidly developing, and further research is still required to fully understand the underlying mechanisms for the metabolic actions of adipokines and their role in obesity-associated HCC.

scholarly journals Current metabolic perspective on malnutrition in obesity: towards more subgroup-based nutritional approaches?

2020 ◽  
Vol 79 (3) ◽  
pp. 331-337 ◽  
Author(s):  
Ellen E. Blaak
Keyword(s):  
Adipose Tissue ◽  
Metabolic Diseases ◽  
Metabolic Health ◽  
Metabolic Phenotype ◽  
Whole Body ◽  
Low Grade ◽  
Plasma Metabolome ◽  
Subcutaneous Adipose ◽  
Low Grade Inflammation

Lifestyle intervention may be effective in reducing type 2 diabetes mellitus incidence and cardiometabolic risk. A more personalised nutritional approach based on an individual or subgroup-based metabolic profile may optimise intervention outcome. Whole body insulin resistance (IR) reflects defective insulin action in tissues such as muscle, liver, adipose tissue, gut and brain, which may precede the development of cardiometabolic diseases. IR may develop in different organs but the severity may vary between organs. Individuals with more pronounced hepatic IR have a distinct plasma metabolome and lipidome profile as compared with individuals with more pronounced muscle IR. Additionally, genes related to extracellular modelling were upregulated in abdominal subcutaneous adipose tissue in individuals with more pronounced hepatic IR, whilst genes related to inflammation as well as systemic low-grade inflammation were upregulated in individuals with primarily muscle IR. There are indications that these distinct IR phenotypes may also respond differentially to dietary macronutrient composition. Besides metabolic phenotype, microbial phenotype may be of importance in personalising the response to diet. In particular fibres or fibre mixtures, leading to a high distal acetate and SCFA production may have more pronounced effects on metabolic health. Notably, individuals with prediabetes may have a reduced response to diet-induced microbiota modulation with respect to host insulin sensitivity and metabolic health outcomes. Overall, we need more research to relate metabolic subphenotypes to intervention outcomes to define more optimal diets for individuals with or predisposed to chronic metabolic diseases.

Butyrate as a Potential Preventive Therapy for Obesity

2019 ◽  
Vol 56 (4) ◽  
pp. 439
Author(s):  
P. Meena Kumari ◽  
S. P. Muthukumar
Keyword(s):  
Barrier Function ◽  
Inflammatory Mediator ◽  
Metabolic Diseases ◽  
Current Knowledge ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Low Grade ◽  
Metabolic Risk ◽  
Metabolic Complications ◽  
Anti Inflammatory

Due to its grave pathological role of obesity, comprehensive research is being continued to find out the causative factors involved in it. Recent advances in this field are increasingly recognized that there is a connection between diet, gut microbiota, intestinal barrier function and the low-grade inflammation that characterize the progression from obesity to metabolic disturbances, making dietary strategies to modulate the intestinal environment is important. In this context, the ability of some Gram-positive anaerobic bacteria to produce the shortchain fatty acid butyrate is impressive. A lower abundance of butyrate-producing bacteria has been associated with metabolic risk in humans. Recent studies suggest that butyrate might have been linked with metabolic risk in humans, and recommend that butyrate might have an anti-inflammatory mediator in metabolic diseases, and the potential of butyrate can alleviate obesity-related metabolic complications, possibly due to its ability to enhance the intestinal barrier function. Endogenous butyrate synthesis, delivery, and absorption by colonocytes have been well studied. Butyrate exerts its function by serving as a histone deacetylase (HDAC) inhibitor or signaling through several G Protein-Coupled Receptors (GPCRs). Latterly butyrate has gained selective attention for its favorable effects on intestinal homeostasis and energy metabolism. With anti-inflammatory properties, butyrate improves intestinal barrier function and mucosal immunity. Growing proof has highlighted the influence of butyrate on obesity. In this review the current knowledge on the features of butyrate, especially its potential effects and mechanisms involved in intestinal health and obesity. Here we review and discuss the potentials of butyrate as an anti-inflammatory mediator in obesity and the potential for dietary interventions increasing intestinal availability of butyrate.

scholarly journals Therapeutic Effects of Quercetin on Inflammation, Obesity, and Type 2 Diabetes

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Shuang Chen ◽  
Hongmei Jiang ◽  
Xiaosong Wu ◽  
Jun Fang
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Capillary Permeability ◽  
Therapeutic Effects ◽  
Low Grade ◽  
Beneficial Effects ◽  
Anti Inflammatory ◽  
Low Grade Inflammation

In previous studies, abdominal obesity has been related to total low-grade inflammation and in some cases has resulted in insulin resistance and other metabolism related disorders such as diabetes. Quercetin is a polyphenol, which is a derivative of plants, and has been shownin vitroas well as in a few animal models to have several potential anti-inflammatory as well as anticarcinogenic applications. The substance has also been shown to aid in the attenuation of lipid peroxidation, platelet aggregation, and capillary permeability. However, further research is called for to gain a better understanding of how quercetin is able to provide these beneficial effects. This manuscript reviewed quercetin’s anti-inflammatory properties in relation to obesity and type 2 diabetes.

scholarly journals THE ROLE OF AMPK AND MTOR IN THE DEVELOPMENT OF INSULIN RESISTANCE AND TYPE 2 DIABETES. THE MECHANISM OF METFORMIN ACTION (literature review)

2016 ◽  
Vol 57 (3) ◽  
pp. 77-90
Author(s):  
V. M. Pushkarev ◽  
L. K. Sokolova ◽  
V. V. Pushkarev ◽  
M. D. Tronko
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Literature Review ◽  
Metabolic Diseases ◽  
Mechanisms Of Action ◽  
Low Grade ◽  
Biochemical Mechanisms ◽  
Low Grade Inflammation

It was analyzed the cellular and molecular links between chronic low-grade inflammation and caused by inflammation insulin resistance and type 2 diabetes. Particular emphasis is placed on the participation of AMPK and mTORC1 in the development of metabolic diseases caused by obesity. A detailed analysis of the biochemical mechanisms of action of the main drug used in the treatment of insulin resistance and type 2 diabetes — metformin.

Sign in / Sign up

Export Citation Format

Share Document