scholarly journals Copper-Fructose Interactions: A Novel Mechanism in the Pathogenesis of NAFLD

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1815 ◽  
Author(s):  
Ming Song ◽  
Miriam Vos ◽  
Craig McClain
Keyword(s):  
Metabolic Syndrome ◽  
Causal Effect ◽  
Critical Role ◽  
Metabolic Effects ◽  
Nonalcoholic Fatty Liver ◽  
Copper Status ◽  
Fructose Intake ◽  
The Metabolic Syndrome ◽  
High Fructose

Compelling epidemiologic data support the critical role of dietary fructose in the epidemic of obesity, metabolic syndrome and nonalcoholic fatty liver disease (NAFLD). The metabolic effects of fructose on the development of metabolic syndrome and NAFLD are not completely understood. High fructose intake impairs copper status, and copper-fructose interactions have been well documented in rats. Altered copper-fructose metabolism leads to exacerbated experimental metabolic syndrome and NAFLD. A growing body of evidence has demonstrated that copper levels are low in NAFLD patients. Moreover, hepatic and serum copper levels are inversely correlated with the severity of NAFLD. Thus, high fructose consumption and low copper availability are considered two important risk factors in NAFLD. However, the causal effect of copper-fructose interactions as well as the effects of fructose intake on copper status remain to be evaluated in humans. The aim of this review is to summarize the role of copper-fructose interactions in the pathogenesis of the metabolic syndrome and discuss the potential underlying mechanisms. This review will shed light on the role of copper homeostasis and high fructose intake and point to copper-fructose interactions as novel mechanisms in the fructose induced NAFLD.

scholarly journals Copper-Fructose Interactions: A Novel Mechanism in the Pathogenesis of NAFLD

2018 ◽  
Author(s):  
Ming Song ◽  
Miriam Vos ◽  
Craig McClain
Keyword(s):  
Metabolic Syndrome ◽  
Causal Effect ◽  
Critical Role ◽  
Metabolic Effects ◽  
Nonalcoholic Fatty Liver ◽  
Copper Status ◽  
Fructose Intake ◽  
The Metabolic Syndrome ◽  
High Fructose

Compelling epidemiologic data support the critical role of dietary fructose in the epidemic of obesity, metabolic syndrome and nonalcoholic fatty liver disease (NAFLD). The metabolic effects of fructose on the development of metabolic syndrome and NAFLD are not completely understood. High fructose intake impairs copper status, and copper-fructose interactions have been well documented in rats. Altered copper-fructose metabolism leads to exacerbated experimental metabolic syndrome and NAFLD. A growing body of evidence has demonstrated that copper levels are low in NAFLD patients. Moreover, hepatic and serum copper levels are inversely correlated with the severity of NAFLD. Thus, high fructose consumption and low copper availability are considered two important risk factors in NAFLD. However, the causal effect of copper-fructose interactions as well as the effects of fructose intake on copper status remain to be evaluated in humans. The aim of this review is to summarize the role of copper-fructose interactions in the pathogenesis of the metabolic syndrome and discuss the potential underlying mechanisms. This review will shed light on the role of copper homeostasis and high fructose intake and point to copper-fructose interactions as novel mechanisms in the fructose induced NAFLD.

scholarly journals Critical role of chemokine (C-C motif) receptor 2 (CCR2) in the KKAy + Apoe −/− mouse model of the metabolic syndrome

Diabetologia ◽  
2011 ◽  
Vol 54 (10) ◽  
pp. 2660-2668 ◽  
Author(s):  
H. G. Martinez ◽  
M. P. Quinones ◽  
F. Jimenez ◽  
C. A. Estrada ◽  
K. Clark ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Mouse Model ◽  
Critical Role ◽  
The Metabolic Syndrome ◽  
Apoe Mouse

Effects of TNF-α antagonist infliximab on fructose-induced metabolic syndrome in rats

2020 ◽  
pp. 096032712096996
Author(s):  
Yasmine A Abdelhamid ◽  
Mohammed F Elyamany ◽  
Muhammad Y Al-Shorbagy ◽  
Osama A Badary
Keyword(s):  
Metabolic Syndrome ◽  
Body Weight ◽  
Adult Population ◽  
Health Issues ◽  
Serum Triglycerides ◽  
Fructose Intake ◽  
The Metabolic Syndrome ◽  
High Fructose ◽  
Affect Body Weight ◽  
Tnf Α

Public health issues have been raised regarding fructose toxicity and its serious metabolic disorders. Deleterious effects of high fructose intake on insulin sensitivity, body weight, lipid homeostasis have been identified. The new millennium has witnessed the emergence of a modern epidemic, the metabolic syndrome (MS), in approximately 25% of the world’s adult population. The current study aimed to investigate the effect of the TNF-α antagonist infliximab on fructose-induced MS in rats. Rats were administered fructose (10%) in drinking water for 12 weeks to induce the experimental MS model. infliximab (5 mg/kg) was injected once weekly intraperitoneally starting on the 13th week for 4 weeks. Increase in body weight, blood glucose level, serum triglycerides (TGs), adiponectin level and blood pressure were present in MS rats. They also prompted increases in serum of leptin, TNF-α, and malondialdehyde (MDA) levels. Treatment with infliximab did not affect body weight, hyperglycemia or hypertension, but decreased serum TGs and increased serum HDL-c levels. Infliximab also decreased adiponectin levels. Surprisingly, infliximab increased MDA above its value in the MS group. These results reflect the fact that infliximab affects the manifestations of MS in rats. Though infliximab reduced TGs, increased HDL-c levels, reversed adiponectin resistance occurred by fructose, the drug failed to combat MS-mediated hyperglycemia, hypertension, and elevated MDA above the insult.

Role of Bile Acids and Bile Acid Receptors in Metabolic Regulation

2009 ◽  
Vol 89 (1) ◽  
pp. 147-191 ◽  
Author(s):  
Philippe Lefebvre ◽  
Bertrand Cariou ◽  
Fleur Lien ◽  
Folkert Kuipers ◽  
Bart Staels
Keyword(s):  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Bile Acids ◽  
Disease Risk ◽  
Critical Role ◽  
Elevated Serum ◽  
Farnesoid X Receptor ◽  
The Metabolic Syndrome ◽  
Increased Risk

The incidence of the metabolic syndrome has taken epidemic proportions in the past decades, contributing to an increased risk of cardiovascular disease and diabetes. The metabolic syndrome can be defined as a cluster of cardiovascular disease risk factors including visceral obesity, insulin resistance, dyslipidemia, increased blood pressure, and hypercoagulability. The farnesoid X receptor (FXR) belongs to the superfamily of ligand-activated nuclear receptor transcription factors. FXR is activated by bile acids, and FXR-deficient ( FXR−/−) mice display elevated serum levels of triglycerides and high-density lipoprotein cholesterol, demonstrating a critical role of FXR in lipid metabolism. In an opposite manner, activation of FXR by bile acids (BAs) or nonsteroidal synthetic FXR agonists lowers plasma triglycerides by a mechanism that may involve the repression of hepatic SREBP-1c expression and/or the modulation of glucose-induced lipogenic genes. A cross-talk between BA and glucose metabolism was recently identified, implicating both FXR-dependent and FXR-independent pathways. The first indication for a potential role of FXR in diabetes came from the observation that hepatic FXR expression is reduced in animal models of diabetes. While FXR−/−mice display both impaired glucose tolerance and decreased insulin sensitivity, activation of FXR improves hyperglycemia and dyslipidemia in vivo in diabetic mice. Finally, a recent report also indicates that BA may regulate energy expenditure in a FXR-independent manner in mice, via activation of the G protein-coupled receptor TGR5. Taken together, these findings suggest that modulation of FXR activity and BA metabolism may open new attractive pharmacological approaches for the treatment of the metabolic syndrome and type 2 diabetes.

scholarly journals Role of Adipokines in the Association between Thyroid Hormone and Components of the Metabolic Syndrome

2019 ◽  
Vol 8 (6) ◽  
pp. 764 ◽  
Author(s):  
Alessandro P. Delitala ◽  
Angelo Scuteri ◽  
Edoardo Fiorillo ◽  
Edward G. Lakatta ◽  
David Schlessinger ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Thyroid Hormone ◽  
Regression Models ◽  
Causal Effect ◽  
Positive Association ◽  
The Metabolic Syndrome ◽  
Standardized Regression Coefficients ◽  
The Impact

Metabolic syndrome (MS) increases cardiovascular risk. The role of thyroid hormone on components of MS is unclear. We analyzed a sample of 4733 euthyroid subjects from SardiNIA study. In female thyrotropin (TSH) was significantly and positively associated with triglycerides (Standardized regression coefficients (β) = 0.081, p < 0.001). Free thyroxine (FT4) was positively associated with HDL (β = 0.056, p < 0.01), systolic blood pressure (SBP) (β = 0.059, p < 0.001), diastolic blood pressure (DBP) (β = 0.044, p < 0.01), and fasting glucose (β = 0.046, p < 0.01). Conversely, FT4 showed a negative association with waist circumference (β = −0.052, p < 0.001). In TSH was positively associated with triglycerides (β = 0.111, p < 0.001) and FT4 showed a positive association with DBP (β = 0.51, p < 0.01). The addition of leptin and adiponectin to the regression models did not substantially change the impact of thyroid hormones on components of MS. Our data suggest that, even within the euthyroid range, excess of truncal adipose tissue is associated with variations in FT4. Leptin and adiponectin exert an additive effect rather than a causal effect. Additional studies should be performed to determine the clinical significance of this finding.

Fructose: a highly lipogenic nutrient implicated in insulin resistance, hepatic steatosis, and the metabolic syndrome

2010 ◽  
Vol 299 (5) ◽  
pp. E685-E694 ◽  
Author(s):  
Mark J. Dekker ◽  
Qiaozhu Su ◽  
Chris Baker ◽  
Angela C. Rutledge ◽  
Khosrow Adeli
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Hepatic Steatosis ◽  
Expression Patterns ◽  
Metabolic Effects ◽  
Leptin Resistance ◽  
Peroxisome Proliferator ◽  
The Metabolic Syndrome ◽  
High Fructose ◽  
The Brain

As dietary exposure to fructose has increased over the past 40 years, there is growing concern that high fructose consumption in humans may be in part responsible for the rising incidence of obesity worldwide. Obesity is associated with a host of metabolic challenges, collectively termed the metabolic syndrome. Fructose is a highly lipogenic sugar that has profound metabolic effects in the liver and has been associated with many of the components of the metabolic syndrome (insulin resistance, elevated waist circumference, dyslipidemia, and hypertension). Recent evidence has also uncovered effects of fructose in other tissues, including adipose tissue, the brain, and the gastrointestinal system, that may provide new insight into the metabolic consequences of high-fructose diets. Fructose feeding has now been shown to alter gene expression patterns (such as peroxisome proliferator-activated receptor-γ coactivator-1α/β in the liver), alter satiety factors in the brain, increase inflammation, reactive oxygen species, and portal endotoxin concentrations via Toll-like receptors, and induce leptin resistance. This review highlights recent findings in fructose feeding studies in both human and animal models with a focus on the molecular and biochemical mechanisms that underlie the development of insulin resistance, hepatic steatosis, and the metabolic syndrome.

The Role of Atypical Antipsychotics in Glucose/Insulin Dysregulation and the Evolving Role of the Psychiatrist in a New Era of Drug Treatment Options

CNS Spectrums ◽  
2004 ◽  
Vol 9 (11) ◽  
pp. 849-861 ◽  
Author(s):  
Anthony Ferraioli ◽  
Kara Lee Shirley ◽  
Panakkal David
Keyword(s):  
Metabolic Syndrome ◽  
Atypical Antipsychotics ◽  
Treatment Options ◽  
Metabolic Effects ◽  
Drug Induced ◽  
New Era ◽  
Metabolic Dysregulation ◽  
The Metabolic Syndrome ◽  
Glucose Dysregulation

ABSTRACTThis article examines the issue of atypical antipsychotics, glucose/insulin, and other metabolic derangements (ie, metabolic syndrome), including a general introduction to the health, concerns of our patients, a review of the literature, possible mechanisms of antipsychotic induced glucose dysregulation, monitoring approaches, and management and prevention of metabolic syndrome. Literature review leads to mechanism hypotheses and risk estimations, leading to guidelines for monitoring and treatment. The patient population suffers from a higher degree of baseline metabolic dysregulation resulting in cardiovascular disease through components of the metabolic syndrome, and this risk increases with administration of atypical antipsychotic medication at different rates, depending on both drug and patient risk factors. The growing knowledge of mechanisms behind drug induced glucose/insulin and other metabolic dysregulation, as well as advances in pharmacogenomics, will help refine drug selection and monitoring for adverse, life-threatening metabolic effects.

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