Metabolic Syndrome: From Global Epidemiology to Individualized Medicine

Batsis, John A.; Nieto-Martínez, Ramfis; López-Jiménez, Francisco

doi:10.1038/sj.clpt.6100355

Cited by 149 publications

(123 citation statements)

References 139 publications

(280 reference statements)

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“…This combination of symptoms, referred to as metabolic syndrome, increases the risk of developing type 2 diabetes mellitus. 1 The consumption of sugar-sweetened beverages and saturated fat has been linked to risks for obesity and diabetes. In recent decades, the intake of sugar-sweetened beverages has clearly increased around the world, 2 and from a recent survey among children, consumption of both sugar-sweetened beverages and saturated fat (especially from snack foods) exceed recommended daily levels.…”

Section: Introductionmentioning

confidence: 99%

A free-choice high-fat high-sugar diet induces glucose intolerance and insulin unresponsiveness to a glucose load not explained by obesity

et al. 2010

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Objectives: In diet-induced obesity, it is not clear whether impaired glucose metabolism is caused directly by the diet, or indirectly via obesity. This study examined the effects of different free-choice, high-caloric, obesity-inducing diets on glucose metabolism. In these free-choice diets, saturated fat and/or a 30% sugar solution are provided in an addition to normal chow pellets. Method: In the first experiment, male rats received a free-choice high-fat high-sugar (HFHS), free-choice high-fat (HF) or a chow diet. In a second experiment, male rats received a free-choice high-sugar (HS) diet or chow diet. For both experiments, after weeks 1 and 4, an intravenous glucose tolerance test was performed. Results: Both the HFHS and HF diets resulted in obesity with comparable plasma concentrations of free fatty acids. Interestingly, the HF diet did not affect glucose metabolism, whereas the HFHS diet resulted in hyperglycemia, hyperinsulinemia and in glucose intolerance because of a diminished insulin response. Moreover, adiposity in rats on the HF diet correlated positively with the insulin response to the glucose load, whereas adiposity in rats on the HFHS diet showed a negative correlation. In addition, total caloric intake did not explain differences in glucose tolerance. To test whether sugar itself was crucial, we next performed a similar experiment in rats on the HS diet. Rats consumed three times as much sugar when compared with rats on the HFHS diet, which resulted in obesity with basal hyperinsulinemia. Glucose tolerance, however, was not affected. Conclusion: Together, these results suggest that not only obesity or total caloric intake, but the diet content also is crucial for the glucose intolerance that we observed in rats on the HFHS diet.

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Section: Introductionmentioning

confidence: 99%

A free-choice high-fat high-sugar diet induces glucose intolerance and insulin unresponsiveness to a glucose load not explained by obesity

et al. 2010

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“…6 The results showed 83 dysregulated genes in the omentum of diabetic obese patients versus non-diabetic obese patients. Overall, 79 of the 83 genes were upregulated.…”

Section: Discussionmentioning

confidence: 99%

“…4,5 Many studies indicate that the morbidity and mortality of obesity are secondary to the insulin resistance syndrome or the metabolic syndrome (MS). 6,7 The MS describes the association between obesity and a host of co-morbidities including hyperglycemia, hypertension, and dyslipidemia. [6][7][8] The third National Health and Nutrition Examination Survey reported that 24% of US adults have MS. 9 As the MS is a major determinant of CV disease risk and predictor of CV mortality, this group needs to be identified and treated.…”

Section: Introductionmentioning

confidence: 99%

“…6,7 The MS describes the association between obesity and a host of co-morbidities including hyperglycemia, hypertension, and dyslipidemia. [6][7][8] The third National Health and Nutrition Examination Survey reported that 24% of US adults have MS. 9 As the MS is a major determinant of CV disease risk and predictor of CV mortality, this group needs to be identified and treated. [7][8][9][10] Theoretically, the inherent nature of adipose tissue may contribute to the pathophysiology of the MS.…”

Section: Introductionmentioning

confidence: 99%

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Identification of cardiovascular genes in omentum from morbidly obese patients with type 2 diabetes

et al. 2010

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Background: The metabolic syndrome describes the association between obesity and co-morbidities including insulin resistance, hypertension, dyslipidemia, and cardiovascular (CV) disease. Adipokines produced from omentum contribute to the risk of CV disease and increase the inflammatory state. This study examines the gene expression differences in the omental tissue of morbidly obese diabetic and non-diabetic patients. Methods: Twenty morbidly obese patients undergoing bariatric surgery were included. Ten patients were diabetic and 10 were non-diabetic. Omental samples were collected intraoperatively and snap frozen. Total RNA was extracted using the Trizol reagent and purified with the RNeasy kit (Qiagen). Microarray experiments were performed using the Affymetrix Gene 1.0 ST array and data was analyzed with the Partek 6.3 program using an unpaired t-test (Po0.05). The gene expression profiles of the diabetic group were compared with the non-diabetic group. Using the Ingenuity program, the gene list generated from the microarray analysis was evaluated and real-time quantitative PCR (qPCR) was used to validate the array data. Results: Compared with the non-diabetic group, the diabetic obese patients showed 79 upregulated genes and 4 downregulated genes with 41.4-fold difference in expression. Ingenuity analysis showed numerous dysregulated genes associated with CV disease including leptin, Von Willebrand factor, P-selectin, angiopoietin-1 (ANGPT1), phospholipase A2 (group VII), and periostin osteoblast specific factor. Microarray results for the earlier mentioned genes were confirmed with qPCR. The results were analyzed with respect to the presence or absence of hyperlipidemia, hypertension, and coronary artery disease. In patients with hyperlipidemia, ANGPT1 and P-selectin were upregulated 1.9-and 2.9-fold, respectively. Conclusions: This microarray analysis of omental tissue from morbidly obese diabetic patients documents a host of upregulated genes related to CV disease. This study provides further evidence that diabetic status predisposes obese patients to a higher risk of developing CV disease.

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“…The prevalence of heart disease is 8.1% in Hispanics and 12.1% in Caucasians (7) and the prevalence of obesity (8), diabetes mellitus, hypertension, and dyslipidemia, is generally higher among Hispanics than Caucasians (7,9).…”

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confidence: 99%

Validity of cardiovascular risk prediction models in Latin America and among Hispanics in the United States of America: a systematic review

Cortés-Bergoderi¹,

Thomas²,

Albuquerque³

et al. 2012

Rev Panam Salud Publica

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. MeSH search terms and domains were related to CVD, prediction rules, Latin America (including the Caribbean), and Hispanics in the United States. Database searches were supplemented by correspondence with experts in the field. 1.68 (95% CI, incident myocardial infarction, 1.36 (95% CI, and CHD death, 1.21 (95% CI,. In Ecuador, a prediction model for CVD and total deaths in hypertensive patients had an area under the curve (AUC) of 0.79 (95% CI,, while the World Health Organization method had an AUC of 0.74 (95% CI,. A study predicting mortality risk in people with Chagas' disease had an AUC of 0.81 (95% CI, According to the World Health Organization (WHO), about 25% of all annual deaths in Latin America are due to cardiovascular diseases (CVD) (2, 3). Cardiovascular risk factors, including obesity, hypertension, hypercholesterolemia, diabetes mellitus, and tobacco use are highly prevalent in Latin America and contribute to three-fourths of its CVD cases (4). The prevalence of most, if not all, of these factors has been steadily increasing in recent years in Latin America, and the trend is expected to continue (3). Results. A total of 1 655 abstracts were identified, of which five cohorts with a total of 13 142 subjects met inclusion criteria. A Mexican cohort showed that the predicted/observed event-rate ratio for coronary heart disease (CHD) according to the Framingham risk score (FRS) wasData regarding CVD burden and trends among Hispanics living in the United States is also alarming and represents the most likely cause of death among this population (5), about 31% of all deaths (6). The prevalence of heart disease is 8.1% in Hispanics and 12.1% in Caucasians (7) and the prevalence of obesity (8), diabetes mellitus, hypertension, and dyslipidemia, is generally higher among Hispanics than Caucasians (7, 9).Estimation of CVD risk using prediction models is considered of high importance to public health since it can aid clinical decision-making, guide therapy, and make interventions more cost effective. It may also help direct public policy when measuring risk trends at the population level (10). In the last few decades, several cardiovascular risk prediction models have been created and introduced worldwide.The Framingham risk score (FRS) was the first of such tools and is arguably the most commonly used model for calculating 10-year risk for CVD events in the world. The FRS has been validated and recalibrated in several different populations, including Australia, China, Japan, New Zealand, Spain, and the United States (11)(12)(13)(14). These studies have shown that the FRS may overestimate CVD risk in some populations and under estimate it in others. Some other prediction models include the Prospective Cardiovascular Munster Heart Study (PROCAM) (15), the Reynolds score (16), and the Systematic Coronary Risk Evaluation system (SCORE) (17).The aim of this study was to assess the use and validity of CVD risk prediction models in Latin America and the Caribbean and among Hispanic populations in the United Sta...

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Metabolic Syndrome: From Global Epidemiology to Individualized Medicine

Cited by 149 publications

References 139 publications

A free-choice high-fat high-sugar diet induces glucose intolerance and insulin unresponsiveness to a glucose load not explained by obesity

A free-choice high-fat high-sugar diet induces glucose intolerance and insulin unresponsiveness to a glucose load not explained by obesity

Identification of cardiovascular genes in omentum from morbidly obese patients with type 2 diabetes

Validity of cardiovascular risk prediction models in Latin America and among Hispanics in the United States of America: a systematic review

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