scholarly journals Dietary modulation of energy homoeostasis and metabolic-inflammation

2019 ◽  
Vol 78 (3) ◽  
pp. 313-318 ◽  
Author(s):  
Helen M Roche
Keyword(s):  
Fatty Acids ◽  
Nutritional Status ◽  
Insulin Signalling ◽  
Cvd Risk ◽  
Metabolic Inflammation ◽  
Pyrin Domain ◽  
Dietary Components ◽  
The Impact ◽  
Receptor Family

Dietary intake and nutritional status is an important environmental factor which can modulate metabolic-inflammation. In recent years, research has made significant advances in terms of understanding the impact of dietary components on metabolic-inflammation, within the context of obesity, type-2 diabetes (T2D) and CVD risk. Our work demonstrated that different fatty acids differentially modulate metabolic-inflammation, initially focusing on Nod-like receptor family, pyrin domain-containing three protein (NLRP3) inflammasome mediated IL-1β biology and insulin signalling. However, the paradigm is more complex, wherein data from the immunology field clearly show that nature of cellular energy metabolism is a key determinant of inflammation. Whilst metabolic-inflammation is a critical biological interaction, there is a paucity of data in relation to the nature and the extent to which nutritional status affects metabolic-inflammation. The complex paradigm will be discussed within the context of if/how dietary components, in particular fatty acids, may modulate obesity, T2D and CVD risk, via inflammatory and metabolic processes.

Nutritional modulation of metabolic inflammation

2017 ◽  
Vol 45 (4) ◽  
pp. 979-985 ◽  
Author(s):  
Anna M. Kirwan ◽  
Yvonne M. Lenighan ◽  
Marcella E. O'Reilly ◽  
Fiona C. McGillicuddy ◽  
Helen M. Roche
Keyword(s):  
Fatty Acids ◽  
Unsaturated Fatty Acids ◽  
Insulin Signalling ◽  
Saturated Fatty Acids ◽  
Dietary Fats ◽  
Peroxisome Proliferator ◽  
Metabolic Inflammation ◽  
Inflammatory Pathways ◽  
Pyrin Domain ◽  
Peroxisome Proliferator Activated Receptors

Metabolic inflammation is a very topical area of research, wherein aberrations in metabolic and inflammatory pathways probably contribute to atherosclerosis, insulin resistance (IR) and type 2 diabetes. Metabolic insults arising from obesity promote inflammation, which in turn impedes insulin signalling and reverse cholesterol transport (RCT). Key cells in the process are metabolically activated macrophages, which up-regulate both pro- and anti-inflammatory pathways in response to lipid spillover from adipocytes. Peroxisome proliferator-activated receptors and AMP-activated protein kinase (AMPK) are regulators of cellular homeostasis that influence both inflammatory and metabolic pathways. Dietary fats, such as saturated fatty acids (SFAs), can differentially modulate metabolic inflammation. Palmitic acid, in particular, is a well-characterized nutrient that promotes metabolic inflammation via the NLRP3 (the nod-like receptor containing a pyrin domain) inflammasome, which is partly attributable to AMPK inhibition. Conversely, some unsaturated fatty acids are less potent agonists of metabolic inflammation. For example, monounsaturated fatty acid does not reduce AMPK as potently as SFA and n-3 polyunsaturated fatty acids actively resolve inflammation via resolvins and protectins. Nevertheless, the full extent to which nutritional state modulates metabolic inflammation requires greater clarification.

scholarly journals Inflammation and metabolism: the role of adiposity in sarcopenic obesity

2020 ◽  
Vol 79 (4) ◽  
pp. 435-447
Author(s):  
G. M. Lynch ◽  
C. H. Murphy ◽  
E. de Marco Castro ◽  
H. M. Roche
Keyword(s):  
Nutritional Status ◽  
Sarcopenic Obesity ◽  
Obesity Risk ◽  
Dietary Interventions ◽  
Double Burden ◽  
Metabolic Inflammation ◽  
Fat Composition ◽  
Dietary Components ◽  
Potential Impact

Sarcopenic obesity is characterised by the double burden of diminished skeletal muscle mass and the presence of excess adiposity. From a mechanistic perspective, both obesity and sarcopenia are associated with sub-acute, chronic pro-inflammatory states that impede metabolic processes, disrupting adipose and skeletal functionality, which may potentiate disease. Recent evidence suggests that there is an important cross-talk between metabolism and inflammation, which has shifted focus upon metabolic-inflammation as a key emerging biological interaction. Dietary intake, physical activity and nutritional status are important environmental factors that may modulate metabolic-inflammation. This paradigm will be discussed within the context of sarcopenic obesity risk. There is a paucity of data in relation to the nature and the extent to which nutritional status affects metabolic-inflammation in sarcopenic obesity. Research suggests that there may be scope for the modulation of sarcopenic obesity with alterations in diet. The potential impact of increasing protein consumption and reconfiguration of dietary fat composition in human dietary interventions are evaluated. This review will explore emerging data with respect to if and how different dietary components may modulate metabolic-inflammation, particularly with respect to adiposity, within the context of sarcopenic obesity.

scholarly journals Nutrients in Fish and Possible Associations with Cardiovascular Disease Risk Factors in Metabolic Syndrome

Nutrients ◽  
2018 ◽  
Vol 10 (7) ◽  
pp. 952 ◽  
Author(s):  
Christine Tørris ◽  
Milada Cvancarova Småstuen ◽  
Marianne Molin
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Fatty Acids ◽  
Fish Consumption ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Protective Role ◽  
Cvd Risk ◽  
The Impact

Non-communicable diseases (NSDs) are responsible for two-thirds of all deaths globally, whereas cardiovascular disease (CVD) alone counts for nearly half of them. To reduce the impact of CVD, targeting modifiable risk factors comprised in metabolic syndrome (e.g., waist circumference, lipid profile, blood pressure, and blood glucose) is of great importance. Beneficial effects of fish consumption on CVD has been revealed over the past decades, and some studies suggest that fish consumption may have a protective role in preventing metabolic syndrome. Fish contains a variety of nutrients that may contribute to health benefits. This review examines current recommendations for fish intake as a source of various nutrients (proteins, n-3 fatty acids, vitamin D, iodine, selenium, and taurine), and their effects on metabolic syndrome and the CVD risk factors. Fatty fish is recommended due to its high levels of n-3 fatty acids, however lean fish also contains nutrients that may be beneficial in the prevention of CVD.

scholarly journals Ruminant and industrial sources of trans-fat and cardiovascular and diabetic diseases

2011 ◽  
Vol 24 (1) ◽  
pp. 111-117 ◽  
Author(s):  
Anne-Laure Tardy ◽  
Béatrice Morio ◽  
Jean-Michel Chardigny ◽  
Corinne Malpuech-Brugère
Keyword(s):  
Risk Factors ◽  
Type 2 Diabetes ◽  
Vaccenic Acid ◽  
Biological Effects ◽  
Epidemiological Data ◽  
Cvd Risk ◽  
Industrial Sources ◽  
Ruminant Meat ◽  
The Impact

The various positional isomers of oleic acid (18 : 1Δ9c or 9c-18 : 1) may have distinct biological effects. Detrimental effects of consumption of industrial trans-fatty acids (TFA) (elaidic acid; 18 : 1Δ9t) from partially hydrogenated vegetable oils on CVD risk factors are well documented. In addition, epidemiological data suggest that chronic consumption of industrial sources of TFA could alter insulin sensitivity and predispose for type 2 diabetes. However, intervention studies on this issue have remained inconclusive. Moreover, very little information is available on the effect of natural sources of TFA (vaccenic acid; 18 : 1Δ11t) coming from dairy products and ruminant meat on the development of CVD and type 2 diabetes. The review focuses on the impact of the consumption of ruminant TFA in relation to cardiovascular risk factors, inflammation and type 2 diabetes.

scholarly journals Omega-3 fatty acids and cardiovascular disease risk: do we understand the relationship?

2009 ◽  
pp. S19-S26 ◽  
Author(s):  
M Vrablík ◽  
M Prusíková ◽  
M Šnejdrlová ◽  
L Zlatohlávek
Keyword(s):  
Cardiovascular Disease ◽  
Fatty Acids ◽  
Disease Risk ◽  
Large Body ◽  
Current Evidence ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Cvd Risk ◽  
Positive Effects ◽  
The Impact

There is a large body of evidence documenting the effects of long-chain polyunsaturated fatty acids with the first double bond at the third position from methyl-terminal (so called omega-3 fatty acids (FAs)) on different components of cardiovascular disease (CVD) risk. However, it may seem the more answers on the topic we learn, the more questions remain to be elucidated. There are three levels of evidence documenting the impact of fish omega-3 FAs on CVD risk. Epidemiological data have shown unequivocally the increased intake of fish is associated with lower CVD morbidity and mortality. Numerous experimental studies have shown (almost always) positive effects of omega-3 FAs on lipoprotein metabolism, coagulation and platelet function, endothelial function, arterial stiffness etc. Most importantly, there are a few prospective clinical endpoint trials (DART, JELIS, GISSI Prevenzione and GISSI-HF) that have examined the impact of omega-3 FAs supplementation on cardiovascular outcomes in different patient populations. Recent meta-analyses of these and other clinical studies have yielded somewhat conflicting results. In this review we will summarize current evidence of omega-3 FAs effects on cardiovascular risk focusing on new data from recent clinical trials as well as possible practical implications for clinical practice.

scholarly journals Dexmedetomidine Inhibits Nlrp3 Inflammasome Priming in BV-2 microglia through the NF-κB Pathway and the ROS-Nlrp3-IL-1β Signaling Axis

2021 ◽  
Author(s):  
Jiawei Xie ◽  
Li Chen ◽  
Yuling Luo ◽  
Jianling Li ◽  
Xianxue Wang ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Inflammatory Factors ◽  
Pyrrolidine Dithiocarbamate ◽  
Neurocognitive Dysfunction ◽  
Pyrin Domain ◽  
Tnf Α ◽  
Signaling Axis ◽  
The Impact ◽  
Necrosis Factor ◽  
Receptor Family

Abstract In the brain, the NOD-like receptor family pyrin domain containing 3 (Nlrp3) inflammasome is mostly expressed in microglia and is considered to be the primary cause of perioperative neurocognitive dysfunction (PND). Dexmedetomidine (Dex), a novel kind of clinical anesthetic with anti-inflammatory properties, has been shown to be effective in preventing PND in surgical patients. However, the mechanism of its anti-neuroinflammatory activity is still quite unclear. We examined the impact of Dex administration on Nlrp3 priming in activated BV-2 cells in this research. To investigate the mechanism by which Dex impacts Nlrp3 priming, we employed the inhibitors pyrrolidine dithiocarbamate (PDTC) and N-acetyl-L-cysteine (NAC) to block the NF-κB p65 and the reactive oxygen species (ROS)-Nlrp3-interleukin (IL)-1β signaling axis, respectively. The results showed that Dex substantially decreased the expression of Nlrp3 and p65 and significantly inhibited the levels of the inflammatory factors IL-1β and tumor necrosis factor (TNF)-α in BV-2 cells stimulated with lipopolysaccharide (LPS). Additionally, when the NF-κB pathway was inhibited by PDTC, Dex could aggravate the downregulation of Nlrp3 and IL-1β in BV-2 cells. What is more, Dex negatively regulated the expression of Nlrp3 and IL-1β in activated BV-2 cells when NAC was added. These results showed that Dex inhibited Nlrp3 priming in LPS-induced BV-2 cells, presumably via blocking the NF-κB pathway and the ROS-Nlrp3-IL-1β signaling axis.

scholarly journals MECHANISMS IN ENDOCRINOLOGY: Metabolic and inflammatory pathways on the pathogenesis of type 2 diabetes

2016 ◽  
Vol 174 (5) ◽  
pp. R175-R187 ◽  
Author(s):  
Andressa Coope ◽  
Adriana S Torsoni ◽  
Licio A Velloso
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Energy Homeostasis ◽  
Metabolic Diseases ◽  
Insulin Signalling ◽  
Inflammatory Factors ◽  
Main Risk Factor ◽  
Metabolic Inflammation ◽  
Insulin Signalling Pathway

Obesity is the main risk factor for type 2 diabetes (T2D). Studies performed over the last 20 years have identified inflammation as the most important link between these two diseases. During the development of obesity, there is activation of subclinical inflammatory activity in tissues involved in metabolism and energy homeostasis. Intracellular serine/threonine kinases activated in response to inflammatory factors can catalyse the inhibitory phosphorylation of key proteins of the insulin-signalling pathway, leading to insulin resistance. Moreover, during the progression of obesity and insulin resistance, the pancreatic islets are also affected by inflammation, contributing to β-cell failure and leading to the onset of T2D. In this review, we will present the main mechanisms involved in the activation of obesity-associated metabolic inflammation and discuss potential therapeutic opportunities that can be developed to treat obesity-associated metabolic diseases.

scholarly journals Effects of a multifactorial ecosustainable isocaloric diet on liver fat in patients with type 2 diabetes: randomized clinical trial

2020 ◽  
Vol 8 (1) ◽  
pp. e001342 ◽  
Author(s):  
Giuseppe Della Pepa ◽  
Claudia Vetrani ◽  
Valentina Brancato ◽  
Marilena Vitale ◽  
Serena Monti ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Fatty Acids ◽  
Fat Content ◽  
Liver Fat ◽  
Liver Fat Content ◽  
Alcoholic Fatty Liver ◽  
Significant Difference ◽  
Dietary Components ◽  
Mufa Diet

IntroductionTreatment options for non-alcoholic fatty liver disease (NAFLD) in patients with type 2 diabetes (T2D) are still a matter of debate. We compared the effects of a diet including different components versus a proven beneficial diet rich in monounsaturated fatty acids (MUFAs) on liver fat in T2D.Research design and methodsAccording to a parallel design, 49 individuals with T2D, overweight/obese, with high waist circumference, 35–75 years-old, in satisfactory blood glucose control with diet or drugs not affecting liver fat content, were randomly assigned to an 8-week isocaloric intervention with a MUFA diet (n=26) or a multifactorial diet rich in fiber, MUFA, n-6 and n-3 polyunsaturated fatty acids, polyphenols, and vitamins D, E, and C (n=23). Before and after the intervention, liver fat content was evaluated by proton magnetic resonance spectroscopy (1H-MRS). 1H-MRS complete data were available for n=21 (MUFA diet) and n=18 (multifactorial diet) participants.ResultsAdherence to dietary interventions was optimal. No significant differences between groups in body weight reduction, plasma glycated hemoglobin, insulin, glucose, lipids and liver enzymes were observed. Liver fat significantly decreased after both the multifactorial diet (9.18%±7.78% vs 5.22%±4.80%, p=0.003) and the MUFA diet (9.47%±8.89% vs 8.07%±8.52%, p=0.027) with a statistically significant difference between changes either in absolute terms (−4.0%±4.5% vs −1.4%±2.7%, p=0.035) or percent (−40%±33% vs −19%±25%, p=0.030).ConclusionsAn isocaloric multifactorial diet including several beneficial dietary components induced a clinically relevant reduction of liver fat in patients with T2D, more pronounced than that induced by simply replacing saturated fat with MUFA. This suggests that the ‘optimal diet’ for NAFLD treatment in T2D should be based on synergic actions of different dietary components on multiple pathophysiological pathways.Trial registration numberNCT03380416.

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