Cardiovascular diseases (CVD) are major causes of death and illness worldwide. In recent decades an increased prevalence of CVD mortality has been reported in low-medium income countries, which has been associated with changes in life styles, deficiencies in health systems and the persistence of social inequities.
The metabolic syndrome comprises a cluster of cardiometabolic risk factors, with insulin resistance and increased adiposity as its central features. Identifying individuals with metabolic syndrome is important due to its association with an increased risk of coronary heart disease and type 2 diabetes mellitus (DM2). Attention has focused on the visceral adipose tissue production of cytokines (adipokines) in metabolic syndrome and DM2, as the levels of the anti-inflammatory adipokine adiponectin are decreased, while proinflammatory cytokines are elevated, creating a proinflammatory state associated with insulin resistance and endothelial dysfunction. We have give special attention to the role of the leptin/adiponectin ratio and we have demonstrated that in individuals with severe coronary artery disease, abdominal obesity (AO) was uniquely related to decreased plasma concentrations of adiponectin and increased leptin levels. 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-I and interleukin-6; these are associated with insulin resistance, DM2, and CVD. In contrast, adiponectin has anti-inflammatory properties and downregulates the expression and release of a number of proinflammatory immune mediators. Its concentrations are negatively regulated by the accumulation of visceral fat, and clinical studies implicate hypoadiponectinemia in the pathogenesis of DM2, coronary artery disease, hypertension, and left ventricular hypertrophy. High concentrations of adiponectin are associated with a decreased risk of coronary artery disease, with an improvement in the differentiation of preadipocytes into adipocytes, and with increased endotelial nitric oxide production. Therefore, it appears that interactions between angiotensin II and leptin/adiponectin imbalance may be important mediators of the elevated risk of developing DM2 and CVD associated with AO.
While in the developed world the incidence of CVD is stabilizing or decreasing and prognosis is improving, incidence is increasing in the developing world. These differences in the global epidemiological profile of CVD may be due to diverse geographical, environmental, demographic, socioeconomic, and ethnic characteristics. One of the explanations for these differences is that the populations of developing countries are more prone to develop cardiovascular and metabolic diseases at lower levels of AO as a result of shorter exposure times to the new lifestyles associated with modernization. The shorter the exposure time, the less adapted the population and the greater the risk of an inflammatory imbalance at lower levels of AO. Ethnic differences in insulin resistance and cardiometabolic disease risk have been described and it has been proposed that these may be the result of differences in circulating adipokines and inflammatory markers associated with ethnic variations in obesity and body fat distribution. In United States (US) significant ethnic differences in adiponectin has been reported, compared with white Americans, African-American men and women, Japanese-American women, and native Hawaiian women have significantly lower levels. Another study conducted in healthy Canadian Aboriginal, Chinese, European, and South Asian adults found that South Asians had the greatest insulin resistance, followed by Aboriginals, Chinese, and Europeans. Plasma adiponectin concentrations were lower in Chinese and South Asians than in Aboriginals and Europeans, and adiponectin was inversely associated with insulin resistance. The authors concluded that ethnic-specific differences in adiponectin may account for the differences in insulin resistance. It was observed that plasma adiponectin concentrations were lower for both Greenlandic Inuit boys and girls, who have a more adverse metabolic profile, than for Danish children. The differences remained after adjustment for body fat percentage, aerobic fitness, age, and puberty. However, in a large study conducted in the United States there were no significant racial or ethnic differences in circulating concentrations of adiponectin, even when adjusted for age, sex, and body composition. This result contrasts with a previous study in adults that reported that circulating concentrations of adiponectin were lower in South Asians even after adjusting for age, sex, and BMI. To explain these contrasting results, it is interesting to consider the proposal that fetal undernutrition produces poor development of structural units such as nephrons, cardiomyocytes, and beta pancreatic cells. These adaptations during fetal programming produce a negative effect in adulthood if food is more abundant in the postnatal period. Nutritional deficiencies during fetal programming through epigenetic mechanisms could affect the expression of genes that result in decreased synthesis of adiponectin. Although it is difficult to establish consistent regional differences, there appear to be considerable differences between developed and developing countries. In Latin America, a Brazilian study reported adiponectin values of 7.11 mg/mL, and we reported concentrations of 5.93 mg/mL in Colombia. In Australian women with metabolic syndrome, however, the values were 13.7 mg/mL, whereas in Indonesian women with metabolic syndrome, the values were much lower (4.9 mg/mL). In US decreased adiponectin concentrations were found in Latino compared with non-Latino white patients with CVD risk and were independent of BMI and other factors known to affect adiponectin and seemed to account for the increased insulin resistance observed in this group. These findings in Latinosare similar to those from studies of adiponectin in other minority ethnic/racial groups in that adiponectin is lower in minority groups than than in white populations. Regional differences in adiponectin values may have an important role in the susceptibility of certain populations to CVD. However, there is a paucity of data to support this, and more research is required.
Foscal, Udes and Latin America Society of Hypertension (LASH), Colombia