Contributed by Sergio Perez-Diaz
Obesity is defined as an excess of body fat tissue. Adipose tissue (white adipose tissue) is the organ whose main function is to store the overflow of energy from the diet. The body mass index (BMI) is a quick formula to know when an individual person is obese, being 25 kg/m2 and 30 kg/m2 the overweight and obesity thresholds, respectively..
Anatomically, the white adipose tissue is present in three big discrete body depots. The big one is the subcutaneous fat tissue (SAT), which stores up to 80% of total body lipids. The most commonly studied, the subcutaneous depot is central-abdominal. Intra-visceral (VAT) fat depot is an inner central-abdominal region that represents 10-20% of total body fat in men and a 5-10% in women. Moreover, there are smaller specialized adipose tissue depots such as, pericardial or intramuscular. Recently was discovered the presence of brown adipose tissue in human adults. Its localization was centered in cervical, perirenal and paravertebral regions with myogenic or trans-differentiation from white adipose tissue origins. Its function is burn fats so knowledge is in focus of researchers to fight against obesity.
High heterogeneity in morphology, cell composition, metabolism or hormonal function exists in each regional depot. Generally, adipocytes are smaller in visceral fat tissue. The non-adipocyte cell number is higher in VAT (with a population of innate system cells, according with the elevated secretion of pro-inflammatory cytokines) than SAT, which contains higher number of precursors of adipocytes and secretion of pro-adiposity adipokines as leptin or adiponectin. The release (lipolysis) and uptake (lipogenesis) of triglycerides of fatty acids to control lipids and carbohydrate homeostasis, is controlled by fat tissue. Adipocytes from SAT have more adipogenesis/lipogenesis markers and lipids stored than VAT adipocytes. The rate of lipolysis is higher in central fat (VAT > SAT) and low in SAT lower body fat.
Genetics, as well as environmental factors has played a role in regional differences of fat storage and distribution in different human populations. It is not difficult to understand the environmental differences between bushmens and inuits in terms of percentage of fat tissue as isolation layer. The size of stores is variable from 5 to 60% of total body weight. There is a worldwide variation of obesity ranging; from India, where 3-4% of the population is obese, until the 80% in some Pacific Island regions. In addition to environmental factors, its susprising how a single mutation in a single gene , as leptin or leptin receptor , lead in rare obesity or how two hours of additional TV Increased 2% of the obesity prevalence.
The evolutionary function of the fat tissue is release nutrients in hunger seasons and stores the nutrients at seasons with excess of food. Today, the genetic obesity factor of each race or region marked by the environment has been blocked by the economic and cultural side of the human society. Excessive caloric intake and so-called junk food in Western countries and absence hunger season in less developed countries made that, the prevalence of obesity in almost all countries was increased in the last years. The world Health organization has estimated that for this year 2015, 2.3 billion and 700 million of people will be overweight or obese respectively.
All obese individuals have in common an elevated percentage of fat tissue. However, fat distribution is highly variable among obese individuals. Recent studies around the world, shown as obese Asians have more central adiposity (VAT and SAT) than Caucasians, and African Americas and Hispanics have relatively less central VAT, but more fat mass than them in percentage. Women have a tendency higher to adiposity than men. In addition, men accumulate more fat in abdominal area and women in lower body. This distribution was canonical named like apple and pear.
About 20-30% of adult population has problems associated with overweight, as Metabolic syndrome (Mets). Classically, Mets is a group of clustered events in individual patients such as: obesity, inflammation, insulin resistance, blood lipids disorders and increased risk of developing cardiovascular disease. Not all obese have the same distribution and size of fat mass and not all obese individuals develop metabolic syndrome. It is known, that different depots lead different quality of life. The general pattern to identifying a patient of Mets, is today unknown but central-abdominal VAT, is the clearest manifestation of Mets.
Now, we know that the SAT (perigluteal in women and elevated ratio, subcutaneous/visceral depots in abdominal fat in men) have “healthy” functions buffering the effect of co-morbidities. Meanwhile, an elevated level of VAT depots raises the risk of suffering metabolic syndrome. For example, the prevalence of diabetes is greater in men than women, likely because femoral SAT storage in women has a healthier role than abdominal fat in men. An interesting view to understand how different depots of Fat tissue changes the prevalence to suffer MetS could be documented in U.S.A. The capacity to gain weight and becoming in obese is lower in American Asians, American Whites and American Blacks is in this order. However, the prevalence of problems associated with the obesity, taken the same BMI in this groups is bigger in American Asians than Blacks. This may be explained because was measure that obese Asians have a low ratio of SAT/VAT than American Blacks. Moreover, MetS is associated with aging. This is due to slower metabolism, together abdominal lipid storage in both sex.
Many theories exist to correlate visceral fat with MetS. The body’s ability to cope with the surplus of calories could determine the susceptibility to developing MetS. If this surplus of energy-dense food or/and lack of physical activity is stored by an insulin-responsive adipose tissue SAT, the gain of weight will be healthy. But, if this surplus is shipped into a dysfunctional SAT unable to expand, this excess of energy will diverted for storage in the visceral fat tissue. The features of VAT, leads abdominal dysfunctional storage of fats and in the end, an ectopic fat depot (as muscle, heart or liver) and presence of clinical Mets.
This knowledge opens a new focus to try to cure, treat or prevent Mets, looking for molecular markers that determine dysfunctional fat tissue and targets to promote the good fat.
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