Causes of Metabolic Syndrome

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DEFINITION OF METABOLIC SYNDROME: CIRCULATION (2004)

These components of the metabolic syndrome constitute a particular combination of what ATP III terms underlying,major, and emerging risk factors. According to ATP III, underlying risk factors for CVD are obesity (especially abdominal obesity), physical inactivity, and atherogenic diet; the major risk factors are cigarette smoking, hypertension, elevated LDL cholesterol, low HDL cholesterol, family history of premature coronary heart disease (CHD), and aging; and the emerging risk factors include elevated triglycerides, small LDL particles, insulin resistance, glucose intolerance, proinflammatory state, and prothrombotic state. For present purposes, the latter 5 components are designated metabolic risk factors. The metabolic syndrome seems to have 3 potential etiological categories: obesity and disorders of adipose tissue; insulin resistance; and a constellation of independent factors (eg, molecules of hepatic, vascular, and immunologic origin) that mediate specific components of the metabolic syndrome. Other factors—aging, proinflammatory state, and hormonal changes—have been implicated as contributors as well.

http://circ.ahajournals.org/content/109/3/433.full


EDITORIAL: NEW TRANSLATIONAL INSIGHTS ON METABOLIC SYNDROME: OBESITY, HYPERTENSION, DIABETES AND BEYOND (2016)

The present research topic involves eleven articles including both reviews and original manuscripts. In a translational perspective, the topic includes both clinical and experimental approaches from different research groups located in several countries, which discuss different aspects of MetS such as hypertension, obesity, diabetes, atherosclerosis, and inflammation. At the present moment, almost 3000 article downloads were performed from researchers all over the world. In this editorial, we highlight important insights from these articles leading to a better comprehension of MetS and its complications.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4901063/


THE NEW INTERNATIONAL DIABETES FEDERATION DEFINTION (2006)

According to the new IDF definition, for a person to be defined as having the metabolic syndrome they must have: Central obesity (defined as waist circumference ≥ 94cm for Europid men and ≥ 80cm for Europid women, with ethnicity specific values for other groups) plus any two of the following four factors: • raised TG level: ≥ 150 mg/dL (1.7 mmol/L), or specific treatment for this lipid abnormality • reduced HDL cholesterol: < 40 mg/dL (1.03 mmol/L*) in males and < 50 mg/dL (1.29 mmol/L*) in females, or specific treatment for this lipid abnormality • raised blood pressure: systolic BP ≥ 130 or diastolic BP ≥ 85 mm Hg, or treatment of previously diagnosed hypertension • raised fasting plasma glucose (FPG) ≥ 100 mg/dL (5.6 mmol/L), or previously diagnosed type 2 diabetes If above 5.6 mmol/L or 100 mg/dL, OGTT is strongly recommended but is not necessary to define presence of the syndrome.

https://www.idf.org/webdata/docs/MetS_def_update2006.pdf


BRITTANIA ACADEMIC (2014)

Metabolic syndrome is common, affecting nearly 25 percent of adults in the United States and the United Kingdom, with the prevalence of the condition being especially high in adults over age 60 and in individuals who are overweight or obese. Insulin resistance, which is believed to play a central role in metabolic syndrome, renders tissues insensitive to insulin and therefore unable to store glucose. Insulin resistance can be caused by obesity, lipodystrophy (atrophy of adipose tissue resulting in fat deposition in non-adipose tissues), physical inactivity, and genetic factors. :::Furthermore, metabolic syndrome can be exacerbated by poor diet (e.g., excessive carbohydrate or fat consumption) in susceptible people and has been associated with Stein-Leventhal syndrome (also called polycystic ovary syndrome), sleep apnea, and fatty liver.

https://www.britannica.com/science/metabolic-syndrome


AMERICAN HEART ASSOCIATION (2015)

In recent years this syndrome has become much more common in the United States. About 34 percent of adult Americans are estimated to have it. Risk of developing metabolic syndrome increases as we age. In the United States, the prevalence of metabolic syndrome is higher in non-Hispanic white men than Mexican-American and non-Hispanic black men. By contrast, it is more common in Mexican American women than non-Hispanic black or non-Hispanic white women. Prevalence of metabolic syndrome is also increasing globally.

https://www.heart.org/idc/groups/heart-public/@wcm/@hcm/documents/downloadable/ucm_300322.pdf


Obesity

IS VISCERAL OBESITY THE CAUSE OF THE METABOLIC SYNDROME? (2009)

Due to its anatomic location and peculiar metabolic, hyperlipolytic activity, the expanded visceral adipose depot is a key correlate of the altered cardiometabolic risk profile observed among individuals with a high‐risk abdominal obesity phenotype. Evidence suggests that this dysmetabolic profile is predictive of a substantially increased risk of coronary heart disease even in the absence of classical risk factors. Finally, a moderate weight loss in initially abdominally obese patients is associated with a preferential mobilization of visceral adipose tissue, which in turn leads to substantial improvements in the metabolic risk profile predictive of a reduced risk of coronary heart disease and of type 2 diabetes.

http://www.tandfonline.com/doi/full/10.1080/07853890500383895?scroll=top&needAccess=true


METABOLIC SYNDROME, OBESITY, AND RELATED RISK FACTORS AMONG COLLEGE MEN AND WOMEN (2012)

The present investigation supports the overwhelming evidence that MbS prevalence is higher among overweight and obese individuals as compared to healthy-weight individuals, thus interventions targeting college-age adults should include weight management objectives. Among older adults, a 2-year adherence to a Mediterranean-style diet has also been shown to reduce the prevalence of the MbS. In a group of obese men and women, moderate weight loss through lifestyle modification alone or in combination with pharmacotherapy has been shown to reduce the prevalence of MbS.

http://www.tandfonline.com/doi/abs/10.1080/07448481.2011.582208?src=recsys&journalCode=vach20


MACROPHAGE GENE EXPRESSION IS RELATED TO OBESITY AND THE METABOLIC SYNDROME IN HUMAN SUBCUTANEOUS FAT AS WELL AS IN VISCERAL FAT (2011)

Our data show that expression of ATM markers is increased with obesity, insulin resistance and occurrence of the metabolic syndrome in human SAT as well as in VAT. This suggests that the worsening of the metabolic status in obese individuals cannot be simply ascribed to ATM-mediated inflammation of visceral fat. Identification of specific ATM populations in different fat depots in individuals with different the metabolic abnormalities is warranted to identify potential pharmacological treatments of obesity and linked disturbances by targeted modulation of macrophage phenotype.

http://link.springer.com/article/10.1007/s00125-010-2014-3


THE CONCEPT OF METABOLIC SYNDROME: CONTRIBUTION OF VISCERAL FAT ACCUMULATION AND ITS MOLECULAR MECHANISM (2011)

In this review article, the important role of visceral fat accumulation in the development of a variety of lifestyle-related diseases is shown, including cardiovascular disease based on our clinical studies using CT scans, and the mechanism of these disorders is discussed, focusing on adipocytokines, especially adiponectin.
The importance of diagnosing metabolic syndrome, in which visceral fat accumulation plays an essential role in the development of multiple risk factors, should be emphasized because lifestyle modification for the reduction of visceral fat may be very effective for the reduction of risks of this type, namely metabolic syndrome in the narrow sense.

https://www.jstage.jst.go.jp/article/jat/18/8/18_7922/_article


Dietary Influence

SINGLE COMPONENT VERSUS MULTICOMPONENT DIETARY GOALS FOR THE METABOLIC SYNDROME: A RANDOMIZED TRIAL (2015)

No clear between-group differences were found, suggesting that a dietary intervention focusing on a targeted fiber goal may be able to achieve clinically meaningful weight loss similar to the widely applied, but more intense, AHA dietary guidelines. The present study also offers insight similar to Spring and colleagues' findings that dietary instructions targeting 1 area of diet may have collateral positive effects on other non-targeted dietary behaviors. However, the ways in which the dynamic of a diet are changed by the addition or removal of a nutrient to the diet are not completely understood and deserve further study. For example, increases in sugar intake were seen at the population level during the time when low-fat diets were highly recommended. A dietary message that focuses on 1 dietary component, such as dietary fiber, is permissive—it encourages an increase in a healthy behavior—versus the AHA diet's restrictive message, which advises persons to limit an unhealthy behavior. Our findings are consistent with several meta analyses that found little to no difference in diet studies comparing low-fat, low-carbohydrate, or Mediterranean diets on weight loss.

http://annals.org/aim/article/2118594/single-component-versus-multicomponent-dietary-goals-metabolic-syndrome-randomized-trial


EFFECT OF A MEDITERRANEAN-STYLE DIET ON ENDOTHELIAL DYSFUNCTION AND MARKERS OF VASCULAR INFLAMMATION IN THE METABOLIC SYNDROME (2004)

In this study, consumption of a Mediterranean-style diet by patients with the metabolic syndrome was associated with improvement of endothelial function and a significant reduction of markers of systemic vascular inflammation. Moreover, participants who followed the intervention diet showed a reduction in the number of the components of the syndrome such that the overall prevalence of the metabolic syndrome was reduced by approximately one half. Because data were adjusted for changes in body weight, the overall reduction in the prevalence of the metabolic syndrome after the intervention is likely to represent a conservative measure. Taken together, these findings suggest that a Mediterranean-style diet is a safe strategy for treatment of the metabolic syndrome and for helping to reduce the associated cardiovascular risk.

http://jamanetwork.com/journals/jama/fullarticle/199488


CARBOHYDRATE NUTRITION, INSULIN RESISTANCE, AND THE PREVALENCE OF THE METABOLIC SYNDROME IN THE FRAMINGHAM OFFSPRING COHORT (2004)

Whole-grain intake, largely attributed to the cereal fiber, is inversely associated with HOMA-IR and a lower prevalence of the metabolic syndrome. :::Dietary glycemic index is positively associated with HOMA-IR and prevalence of the metabolic syndrome. Given that both a high cereal fiber content and lower glycemic index are attributes of whole-grain foods, recommendation to increase whole-grain intake may reduce the risk of developing the metabolic syndrome.

http://care.diabetesjournals.org/content/27/2/538.full


AWAY-FROM-HOME FAMILY DINNER SOURCES AND ASSOCIATIONS WITH WEIGHT STATUS, BODY COMPOSITION, AND RELATED BIOMARKERS OF CHRONIC DISEASE AMONG ADOLESCENTS AND THEIR PARENTS (2012)

Present study findings indicate that the odds of overweight/obesity are considerably greater when families report at least one weekly away-from-home dinner purchase. Mean percent body fat and CVD biomarkers are also considerably greater with weekly purchases of family dinner from fast-food restaurants and takeout sources. Future research should investigate these associations with an ethnically and demographically diverse sample of families using validated measures and a prospective, longitudinal study design.

http://www.sciencedirect.com/science/article/pii/S0002822311016579


RELATIONSHIP BETWEEN ULTRA-PROCESSED FOODS AND METABOLIC SYNDROME IN ADOLESCENTS FROM A BRAZILIAN FAMILY DOCTOR PROGRAM (2012)

Crude analysis showed higher average daily intakes of energy, carbohydrates and ultra-processed foods among adolescents with MetS. After statistical adjustment, the intake of ultra-processed foods (≥3rd quartile) remained associated with MetS (prevalence ratio = 2·5; P = 0·012). High consumption of ultra-processed foods was associated with the prevalence of MetS in this adolescents group.

https://doi.org/10.1017/S1368980011001571


DIETARY FIBER AND NUTRIENT DENSITY ARE INVERSELY ASSOCIATED WITH THE METABOLIC SYNDROME IN US ADOLESCENTS (2011)

The results of this study indicate that a higher intake of dietary fiber is significantly associated with lower odds of the MetS in adolescents, whereas low intakes of saturated fat or dietary cholesterol were not associated with MetS. A potential clinical implication of these findings supports the notion of an inclusive rather than an exclusionary dietary paradigm. The association of a high FI with a significantly lower prevalence of MetS highlights the importance of a dietary pattern that includes fiber-rich plant-based foods, and the limitation of defining a heart-healthy diet based solely on a low total fat, saturated fat, and cholesterol intake.

https://www.ncbi.nlm.nih.gov/pubmed/22027051


Non-Alcoholic Fatty Liver Disease

NAFL AS A CAUSE AND A CONSEQUENCE OF METABOLIC SYNDROME (2014)

Metabolic syndrome is a cluster of metabolic abnormalities that identifies people at risk of diabetes and cardiovascular disease, whereas non-alcoholic fatty liver disease (NAFLD) is defined as a disorder with excess fat in the liver due to non-alcoholic causes. Two key components of metabolic syndrome, glucose and triglycerides, are overproduced by the fatty liver. The liver is therefore a key determinant of metabolic abnormalities. The prevalence of both metabolic syndrome and NAFLD increases with obesity. Other acquired causes for both disorders include excessive intake of simple sugars and physical inactivity. Both disorders predict type 2 diabetes, cardiovascular disease, non-alcoholic steatohepatitis (NASH), and hepatocellular carcinoma. Because metabolic syndrome can be defined in many different ways, NAFLD might be a more direct predictor of these diseases. Half of people with NAFLD carry at least one variant (G) allele at rs738409 in the PNPLA3 gene, which is associated with high liver fat content. Steatosis in PNPLA3-associated NAFLD is not accompanied by features of metabolic syndrome. All forms of NAFLD increase the risk of NASH, cirrhosis, and hepatocellular carcinoma.

https://www.ncbi.nlm.nih.gov/pubmed/24731669


IDENTIFICATION OF RECIPROCAL CAUSALITY BETWEEN NON-ALCOHOLIC FATTY DISEASE AND METABOLIC SYNDROME BY A SIMPLIFIED BAYNESIAN NETWORK IN A CHINESE POPULATION (2015)

To the best of our knowledge, this has been the first large-scale bidirectional longitudinal cohort study to clarify the reciprocal causality between NAFLD and MetS within the same study population. We confirmed that NAFLD could be both a cause and consequence of MetS in this bidirectional longitudinal cohort from a section of the Chinese population. As for the results of the longitudinal association between NAFLD and MetS, similar results have been found in other national and regional populations for the temporal sequence of NAFLD to MetS and MetS to NAFLD. Furthermore, we found that the effect of MetS on NAFLD was higher than that of NAFLD on MetS in reciprocal causality between NAFLD and MetS.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4593152/

Metabolic Syndrome In Children

WHAT IS METABOLIC SYNDROME AND WHY ARE CHILDREN GETTING IT? (2013)

Metabolic syndrome is a complex phenotype that correlates with obesity, but nonetheless appears to be distinct from it. The fact that children can develop metabolic syndrome suggests that while obesity and aging contribute to the syndrome, it is unlikely that they are initiating factors. The fact that children around the world are getting heavier and developing the syndrome argues against genetics. More likely, the environment plays a major role, in particular the typical Western diet, which has now been adopted globally due to palatability and price. This review outlines the potential instigators and their pathophysiological mechanisms, which starts with mitochondrial overload and results in de novo lipogenesis, insulin resistance, ROS formation, peroxisomal dysfunction, and ER stress and the UPR.

http://onlinelibrary.wiley.com/doi/10.1111/nyas.12030/full


SHBG GENE POLYMORPHISM (RS1799941) ASSOCIATES WITH METABOLIC SYNDROME IN CHILDREN AND ADOLESCENTS (2015)

Originally, MetS in children was defined as a direct consequence of childhood obesity. However, cardio metabolic (CM) risk traits such as high blood pressure and dyslipidemia are now common in children even in the absence of obesity. Furthermore, ethnic variations exist in the distribution of CM risk traits in children. In a previous study comparing children from Ankara, Turkey to the Bogalusa Heart Study population, we reported that dyslipidemia and high blood pressure were highly prevalent in children from Turkey even in the absence of obesity. CM risk is also affected by sex hormone levels in children through regulation of lipids. Both sex hormone and sex hormone binding globulin (SHBG) levels are associated with lipid levels and insulin resistance in children and adolescents.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4380117/


EFFECTS OF RECOMMENDATIONS TO FOLLOW THE DIETARY APPROACHES TO STOP HYPERTENSION (DASH) DIET V. USUAL DIETARY ADVICE ON CHILDHOOD METABOLIC SYNDROME: A RANDOMISED CROSS-OVER CLINICAL TRIAL (2013)

The DASH group was recommended to consume a diet rich in fruits, vegetables and low-fat dairy products and low in saturated fats, total fats and cholesterol. UDA consisted of general oral advice and written information about healthy food choices based on healthy MyPlate. Compliance was assessed through the quantification of plasma vitamin C levels. Compared with the UDA group, the DASH group experienced a significant reduction in the prevalence of the MetS and high blood pressure. Recommendations to follow the DASH eating pattern for 6 weeks among adolescent girls with the MetS led to reduced prevalence of high blood pressure and the MetS and improved diet quality compared with UDA. This type of healthy diet can be considered as a treatment modality for the MetS and its components in children.
Fast Food Intake Increases the Incidence of Metabolic Syndrome in Children and Adolescents: Tehran Lipid and Glucose Study (2015): In the current study, children and adolescents showed undesirable effects of fast food intakes on incidence of MetS. In addition, positive associations were found between fast food consumption and increased risk of abdominal obesity and hypertriglyceridemia. Sausage, French fries, and pizza consumption were associated with higher risk of incident MetS. Our findings are in agreement with those of cross-sectional studies of fast food and MetS.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4598125/


Pre-Natal Factors

THE DEVELOPMENTAL ORIGINS OF THE METABOLIC SYNDROME (2004)

Both epidemiological and clinical evidence suggest relationships between the antenatal environment and the risk of developing insulin resistance and associated cardiovascular disease (part of the metabolic syndrome) in middle age. However, interpretation of these findings has been controversial. Recent experimental observations provide considerable evidence for a causal model linking adaptive responses to early environmental cues and the later risk of disease. Evolutionary and life history theory provide possible explanations of why these phenomena have persisted and how they might cause disease. In this article, we review the clinical and experimental perspectives on the ‘developmental origins of disease’ model in the context of these new concepts.

http://www.sciencedirect.com/science/article/pii/S1043276004000578


MECHANISMS OF DEVELOPMENTAL PROGRAMMING OF THE METABOLIC SYNDROME AND RELATED DISORDERS (2010)

There is consistent epidemiological evidence linking low birth weight, preterm birth and adverse fetal growth to an elevated risk of the metabolic syndrome (obesity, raised blood pressure, raised serum triglycerides, lowered serum high-density lipoprotein cholesterol and impaired glucose tolerance or insulin resistance) and related disorders. This “fetal or developmental origins/programming of disease” concept is now well accepted but the “programming” mechanisms remain poorly understood. We reviewed the major evidence, implications and limitations of current hypotheses in interpreting developmental programming and discuss future research directions.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3083886/


DEVELOPMENTAL PROGRAMMING OF THE METABOLIC SYNDROME BY MATERNAL NUTRITIONAL IMBALANCE: HOW STRONG IS THE EVIDENCE FROM EXPERIMENTAL MODELS IN MAMMALS? (2004)

Population-based studies have suggested that predisposition to the metabolic syndrome may be acquired very early in development through inappropriate fetal or neonatal nutrition. Further evidence for developmental programming of the metabolic syndrome has now been suggested by animal studies in which the fetal environment has been manipulated through altered maternal dietary intake or modification of uterine artery blood flow. This review examines these studies and assesses whether the metabolic syndrome can be reliably induced by the interventions made.

https://www.ncbi.nlm.nih.gov/pubmed/15459241


Insulin Resistance

AMPK, INSULIN RESISTANCE, AND THE METABOLIC SYNDROME (2013)

Insulin resistance (IR) and hyperinsulinemia are hallmarks of the metabolic syndrome, as are central adiposity, dyslipidemia, and a predisposition to type 2 diabetes, atherosclerotic cardiovascular disease, hypertension, and certain cancers. Regular exercise and calorie restriction have long been known to increase insulin sensitivity and decrease the prevalence of these disorders. The subsequent identification of AMP-activated protein kinase (AMPK) and its activation by exercise and fuel deprivation have led to studies of the effects of AMPK on both IR and metabolic syndrome–related diseases. In this review, we evaluate this body of literature, with special emphasis on the hypothesis that dysregulation of AMPK is both a pathogenic factor for these disorders in humans and a target for their prevention and therapy.

http://www.jci.org/articles/view/67227?utm_campaign=impact_2013_july&utm_content=short_url&utm_medium=pdf&utm_source=impact


ADIPONECTIN AND ADIPONECTIN RECEPTORS IN INSULIN RESISTANCE, DIABETES, AND THE METABOLIC SYNDROME (2006)

The adiponectin receptors, AdipoR1 and AdipoR2, which mediate the antidiabetic metabolic actions of adiponectin, have been cloned and are downregulated in obesity-linked insulin resistance. Upregulation of adiponectin is a partial cause of the insulin-sensitizing and antidiabetic actions of thiazolidinediones. Therefore, adiponectin and adiponectin receptors represent potential versatile therapeutic targets to combat obesity-linked diseases characterized by insulin resistance. This Review describes the pathophysiology of adiponectin and adiponectin receptors in insulin resistance, diabetes, and the metabolic syndrome.

http://www.jci.org/articles/view/29126/


HEPATIC INSULIN RESISTANCE, METABOLIC SYNDROME AND CARDIOVASCULAR DISEASE (2009)

Insulin resistance is thought to be the fundamental cause of the metabolic syndrome. Although genetic factors should be considered in the etiology of insulin resistance, it is clear that environmental factors leading to visceral obesity play a greater role. Resistance to insulin action in the liver, either due to genetic factors or obesity, results in an array of metabolic disorders that ultimately have deleterious effects on endothelial cells, leading to atherosclerosis. Hepatic insulin resistance has a major role in eliciting the key components of MetS such as dyslipidemia, hyperglycemia, and development of pro-inflammatory and pro-thrombotic states, all of which have been shown to directly promote atherosclerosis.

http://www.sciencedirect.com/science/article/pii/S0009912009002513


INSULIN SIGNALLING, RESISTANCE, AND METABOLIC SYNDROME: INSIGHTS FROM MOUSE MODELS INTO DISEASE MECHANISMS (2014)

Mouse studies have demonstrated that Akt inactivation and Foxo1 activation following the suppression of IRS1 and IRS2 act as a fundamental mechanism for insulin resistance, which occurs in insulin-responsive tissues, impairing systemic glucose and lipid homeostasis and body weight control and serving as an important mechanism for the development of metabolic syndrome. Metabolic syndrome includes insulin resistance in different organs of the body, such as the brain, liver, pancreas, adipose tissue, muscle, and the cardiovascular system. The IRS→Akt→Foxo1 signaling cascade and its regulatory network require further exploration under different cellular and environmental contexts.

http://joe.endocrinology-journals.org/content/220/2/T1.full#sec-27


Ethnicity

ETHNIC DIFFERENCES IN THE PREVALENCE OF METABOLIC SYNDROME: RESULTS FROM A MULTI-ETHNIC POPULATION-BASED SURVEY IN MALAYSIA (METABOLIC SYNDROME, ETHNICITY AND AGE) (2012)

The overall prevalence of metabolic syndrome in Malaysia was high, with marked differences across ethnicities. Ethnic Chinese had the lowest prevalence of metabolic syndrome, while ethnic Indians had the highest. Indigenous Sarawakians showed a marked increase in metabolic syndrome at young ages.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3460855/


A COMPLEX WEB OF RISKS FOR METABOLIC SYNDROME: RACE/ETHNICITY, ECONOMICS, AND GENDER (2007)

The prevalence of metabolic syndrome was lower among black women than white women, primarily because the prevalence of elevated triglycerides was lower among blacks than whites. Mexican-American women had the highest prevalence of metabolic syndrome overall, with 37% of these women meeting the criteria. Mexican-American women had the highest prevalence of elevated glucose and low HDL, but approximately the same prevalence of elevated triglycerides as white women. Mexican-American and black women had equally high rates of abdominal obesity, and Mexican-American women had the lowest prevalence of hypertension.

http://www.sciencedirect.com/science/article/pii/S0749379707002310


ETHNIC DISPARITIES IN THE PREVALENCE OF METABOLIC SYNDROME AND ITS RISK FACTORS IN THE SURINAME HEALTH STUDY: A CROSS-SECTIONAL POPULATION STUDY (2016)

The prevalence of the MetS in Suriname was higher than that in European countries, but comparable to prevalences in South Asia. The prevalence was the highest among the Hindustanis, followed by the Amerindians and Javanese. Central obesity and low HDL-C, especially in women, had the highest prevalence among the components of MetS. The prevalence of the different components of MetS varied between ethnicities. The observed heterogeneity in the associations with the risk factors and MetS among ethnicities did not influence the differences in OR for MetS among ethnic groups. The observed differences suggest that ethnicity should be considered in screening and for the development of preventive strategies for MetS.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5168639/


Hormones

SERUM LEPTIN IS ASSOCIATED WITH METABOLIC SYNDROME IN OBESE AND NON-OBESE KOREAN POPULATIONS (2009)

Our study demonstrates that serum leptin is associated with metabolic syndrome in the adult Korean population. Subjects with high leptin levels had a higher prevalence of metabolic risk factors than those with lower levels. Leptin was found to be correlated with several components from the cluster of cardiovascular risk factors and increased with the increased risk of metabolic syndrome. Moreover, the correlation between serum leptin levels and metabolic syndrome in the two groups, obese and non-obese participants, were observed to be similar.

http://www.sciencedirect.com/science/article/pii/S002604950900345X


THE ROLE OF LEPTIN/ADIPONECTIN RATIO IN METABOLIC SYNDROME AND DIABETES (2014)

Leptin/adiponectin imbalance was associated with increased waist circumference and a decreased vascular response to acetylcholine and increased vasoconstriction due to angiotensin II. Leptin and adiponectin have opposite effects on subclinical inflammation and insulin resistance. Leptin upregulates proinflammatory cytokines such as tumor necrosis factor-α and interleukin-6; these are associated with insulin resistance and type 2 diabetes mellitus. In contrast, adiponectin has anti-inflammatory properties and downregulates the expression and release of a number of proinflammatory immune mediators. Therefore, it appears that interactions between angiotensin II and leptin/adiponectin imbalance may be important mediators of the elevated risk of developing type 2 diabetes mellitus and cardiovascular diseases associated with abdominal obesity.

https://www.ncbi.nlm.nih.gov/pubmed/25389999


CIRCULATING IRISIN IN RELATION TO INSULIN RESISTANCE AND THE METABOLIC SYNDROME (2013)

Irisin is associated with increased risk of MetS, cardiometabolic variables, and CVD in humans, indicating either increased secretion by adipose/muscle tissue and/or a compensatory increase of irisin to overcome an underlying irisin resistance in these subjects.

http://press.endocrine.org/doi/abs/10.1210/jc.2013-2373


Microbiome

TRANSFER OF INTESTINAL MICROBIOTA FROM LEAN DONORS INCREASES INSULIN SENSITIVITY IN INDIVIDUALS WITH METABOLIC SYNDROME (2012)

Six weeks after infusion of microbiota from lean donors, insulin sensitivity of recipients increased (median rate of glucose disappearance changed from 26.2 to 45.3 mol/kg/min; P < .05) along with levels of butyrate-producing intestinal microbiota. Intestinal microbiota might be developed as therapeutic agents to increase insulin sensitivity in humans.

http://www.sciencedirect.com/science/article/pii/S001650851200892X


NUTRITION, THE GUT MICROBIOME AND THE METABOLIC SYNDROME (2013)

In this review we discuss the complexity surrounding the interactions between diet and the gut microbiota, and their connection to obesity. :::Furthermore, we review the literature on the effects of probiotics and prebiotics on the gut microbiota and host metabolism, focussing primarily on their anti-obesity potential.

http://www.sciencedirect.com/science/article/pii/S1521691813000711


OBESITY, METABOLIC SYNDROME, AND MICROBIOTA: MULTIPLE INTERACTIONS (2010)

Diet may have a fundamental effect on the composition of our microbiota. Early studies highlight the importance for specific diets such as a high-fat diet, which efficiently and very rapidly (within a single day) modulates the gut microbiome. The innate immune system might influence the metabolic syndrome and obesity, as mice deficient in Toll-like receptor 5 develop hyperphagia, become obese and insulin resistant. Importantly, transmission of the microbiota from these mice to healthy mice results in features of the metabolic syndrome. Available data suggest that the microbiota might play a role in the development of metabolic syndrome and obesity.

http://journals.lww.com/jcge/Abstract/2010/09001/Obesity,_Metabolic_Syndrome,_and_Microbiota_.5.aspx