Diabetes Mellitus (DM) is an inflammatory clinical entity with different mechanisms involved in its physiopathology. Among these, the dysfunction of the gut microbiota stands out. Currently, it is understood that lipid products derived from the gut microbiota are capable of interacting with cells from the immune system and have an immunomodulatory effect. In the presence of dysbiosis, the concentration of lipopolysaccharides (LPS) increases, favoring damage to the intestinal barrier. Furthermore, a pro-inflammatory environment prevails, and a state of insulin resistance and hyperglycemia is present. Conversely, during eubiosis, the production of short-chain fatty acids (SCFA) is fundamental for the maintenance of the integrity of the intestinal barrier as well as for immunogenic tolerance and appetite/satiety perception, leading to a protective effect. Additionally, it has been demonstrated that alterations or dysregulation of the gut microbiota can be reversed by modifying the eating habits of the patients or with the administration of prebiotics, probiotics, and symbiotics. Similarly, different studies have demonstrated that drugs like Metformin are capable of modifying the composition of the gut microbiota, promoting changes in the biosynthesis of LPS, and the metabolism of SCFA.

Introduction Subclinical hypothyroidism (ScH) is an endocrine alteration that is related to cardiovascular risk factors, including those categorized as components of the Metabolic Syndrome (MS). However, findings in prior reports regarding an association between these alterations are inconsistent. The purpose of this study was to determine the relationship between both entities in adult subjects from Maracaibo City, Venezuela. Materials and Methods The Maracaibo City Metabolic Syndrome Prevalence Study is a descriptive, cross-sectional study with random and multistage sampling. In this substudy, 391 individuals of both genders were selected and TSH, free T3, and free T4 tests were performed as well as a complete lipid profile, fasting glycaemia, and insulin blood values. ScH was defined according to the National Health and Nutrition Examination Survey (NHANES) criteria: high TSH (≥4.12mUI/L) and normal free T4 (0.9-1,9 ng/dL) in subjects without personal history of thyroid disease. MS components were defined according to IDF/AHA/NHLBI/WHF/IAS/IASO-2009 criteria. A multiple logistic regression analysis was used to assess the relationship between MS components and ScH diagnosis. Results Of the evaluated population, 10.5% (n=41) was diagnosed with ScH, with a higher prevalence in women (female: 13.6% versus male: 7.7%; χ2=3.56, p=0.05). Likewise, 56.1% (n=23) of the subjects with ScH were diagnosed with MS (χ2=4.85; p=0.03), being hyperglycemia the main associated criterion (χ2=11.7; p=0.001). In multivariable analysis, it was observed that the relationship was exclusive with the presence of type 2 diabetes mellitus (T2DM) OR: 3.22 (1.14-9.14); p=0.03. Conclusion The relationship between ScH and MS in our population is dependent on the presence of hyperglycemia, specifically T2DM diagnosis, findings that vary from those previously reported in Latin American subjects.

Metabolic syndrome (MS) is a set of cardio-metabolic risk factors that includes central obesity, hyperglycemia, hypertension, and dyslipidemias. The syndrome affects 25% of adults worldwide. The definition of MS has evolved over the last 80 years, with various classification systems and criteria, whose limitations and benefits are currently the subject of some controversy. Likewise, hypotheses regarding the etiology of MS add more confusion from clinical and epidemiological points of view. The leading suggestion for the pathophysiology of MS is insulin resistance (IR). IR can affect multiple tissues and organs, from the classic “triumvirate” (myocyte, adipocyte, and hepatocyte) to possible effects on organs considered more recently, such as the central nervous system (CNS). Mild cognitive impairment (MCI) and Alzheimer’s disease (AD) may be clinical expressions of CNS involvement. However, the association between MCI and MS is not understood. The bidirectional relationship that seems to exist between these factors raises the questions of which phenomenon occurs first and whether MCI can be a precursor of MS. This review explores shared pathophysiological mechanisms between MCI and MS and establishes a hypothesis of a possible MCI role in the development of IR and the appearance of MS.

Background. Lipoprotein(a) [Lp(a)] is a known risk factor for cardiovascular disease, yet its influence on metabolic syndrome (MS) is still controversial. The purpose of this study was to assess the impact generated by this diagnosis in serum Lp(a) concentrations. Materials and Methods. A total of 1807 subjects of both genders (55.3% women and 44.7% men) belonging to the Maracaibo City Metabolic Syndrome Prevalence Study were evaluated. Results were expressed as Mean ± SD, determining differences through Student's t-test and One-Way ANOVA test. Multiple logistic regression models were utilized for analyzing factors associated with elevated serum Lp(a) levels and MS. Total cholesterol and LDL-C were corrected according to Lp(a)-Cholesterol when necessary. Results. No differences were found in Lp(a) values between genders; P = 0,292. The association between MS and the classification of Lp(a) was statistically significant (χ 2 = 28.33; P < 0,0001), with greater levels in subjects with this diagnosis. In the univariate analysis, subjects with each of the separate diagnostic criteria showed higher serum Lp(a) concentrations, except for hyperglycemia. Conclusions. Lp(a) values exhibit important variations regarding MS and each of its components. Impaired fasting glucose appeared as a protecting factor against elevated Lp(a) concentrations, whereas its association with LDL-C and hs-CRP suggests a potential pro-inflammatory role.

Background: A growing body of evidence suggests that cigarette smoking can cause the onset of metabolic syndrome prior to cardiovascular diseases. Therefore, the objective of this study was to evaluate the relationship between smoking habit and metabolic syndrome components in an adult population from Maracaibo city, Venezuela. Methods: The Maracaibo City Metabolic Syndrome Prevalence Study is a descriptive, cross-sectional study with random and multi-stage sampling. In this sub-study, 2212 adults from both genders were selected. On the basis of their medical background, they were classified as smokers, non-smokers and former smokers. Metabolic syndrome was defined according to Harmonizing 2009 criteria, using population-specific abdominal circumference cut-off points. The association between risk factors was evaluated using a logistic regression model. Results: In the studied population, 14.8% were smokers, 15.4% were former smokers. In the multivariate analysis, the presence of metabolic syndrome (smokers: OR, 1.54; 95% CI, 1.11–2.14; p=0.010) and its components were related to cigarette smoking, with the exception of hyperglycemia. High blood pressure was inversely associated with current smoking status (smokers: OR, 0.70 (0.51–0.95); p=0.025). Conclusion: Cigarette smoking represents a related factor with metabolic syndrome, being associated with low high-density lipoprotein-cholesterol, increased abdominal circumference and elevated triacylglyceride levels. Former smokers did not present a greater risk for developing this metabolic disease when compared to non-smokers. The effect of avoiding this habit should be evaluated in future studies in our population.