Nutrition, insulin resistance and dysfunctional adipose tissue determine the different components of metabolic syndrome

Abstract

Obesity is an excessive accumulation of body fat that may be harmful to health. Today, obesity is a major public health problem, affecting in greater or lesser proportion all demographic groups. Obesity is estimated by body mass index (BMI) in a clinical setting, but BMI reports neither body composition nor the location of excess body fat. Deaths from cardiovascular diseases, cancer and diabetes accounted for approximately 65% of all deaths, and adiposity and mainly abdominal adiposity are associated with all these disorders. Adipose tissue could expand to inflexibility levels. Then, adiposity is associated with a state of low-grade chronic inflammation, with increased tumor necrosis factor-α and interleukin-6 release, which interfere with adipose cell differentiation, and the action pattern of adiponectin and leptin until the adipose tissue begins to be dysfunctional. In this state the subject presents insulin resistance and hyperinsulinemia, probably the first step of a dysfunctional metabolic system. Subsequent to central obesity, insulin resistance, hyperglycemia, hypertriglyceridemia, hypoalphalipoproteinemia, hypertension and fatty liver are grouped in the so-called metabolic syndrome (MetS). In subjects with MetS an energy balance is critical to maintain a healthy body weight, mainly limiting the intake of high energy density foods (fat). However, high-carbohydrate rich (CHO) diets increase postprandial peaks of insulin and glucose. Triglyceride-rich lipoproteins are also increased, which interferes with reverse cholesterol transport lowering high-density lipoprotein cholesterol. In addition, CHO-rich diets could move fat from peripheral to central deposits and reduce adiponectin activity in peripheral adipose tissue. All these are improved with monounsaturated fatty acid-rich diets. Lastly, increased portions of ω-3 and ω-6 fatty acids also decrease triglyceride levels, and complement the healthy diet that is recommended in patients with MetS.

Adipokine profile in patients with anorexia nervosa

“…Moreover, it has also been established that partial weight restoration leads to greater fat mass deposition in the trunk region than other body regions in adolescent females. Furthermore, after short-term weight restoration, whether partial or complete, despite lean stature, adults show a central adiposity phenotype when compared to healthy agematched controls [37]. A temporary predominance of trunk fat depots in connection with biological activity of visceral adipose tissue may result in disturbed adipokine secretion and activity, and consequently may predispose to insulin resistance, Generally, adiponectin concentration is closely and inversely related to insulin concentration and insulin resistance, and mirrors the whole body insulin sensitivity.…”

“…In fact, adipose tissue redistribution in the course of AN results in relative abdominal obesity with metabolic consequences that may include insulin resistance [37].…”

Assessment of the Hypoglycemic Effects of the Aqueous Extracts of Bauhinia forficata in Wistar Rats Fed with a High Fat Diet

“…Group D showed significant increase in body mass gain 78 at 120 day-old compare to group C (Fig 2a). The increased energy gain presented is naturally expected from increased fat deposits, especially visceral fat, which is typically proven in resistance insulin and DM (Paniagua, 2016). The D+I group revealed AqE of B. forficata gradative normalize body mass ( Figure 2b).…”

Associated Risks of Obesity and/or Metabolic Syndrome with Intra-operative or Post-Operative Occurrences in Patients with Open Ventral Hernia Repair

“…Inflammation and oxidative stress accompanying adipocytes hypertrophy secondary to surplus of fat storage lead to excess release of proinflammatory cytokines like interleukin-1 (IL-1), interleukin-6 (IL-6) (one third of total IL-6 concentration come from adipose tissue), Post-Operative Occurrences in Patients with Open Ventral Hernia Repair C-reactive protein and tumor-necrosis factor alpha (TNF-α), resulting in low-grade chronic inflammation, which begins in adipose tissue and eventually reaches the circulation and other organs. [7] Since MS pathogenesis theory involves release and over expression of above mentioned pro-inflammatory cytokines (IL-1, IL-6, TNF-α and CRP) which also paly important role in local and systemic inflammatory response to injury, a hypothesis has been made that there might be some influence of these changes on the intra-operative body response to surgical trauma or on the development of early postoperative wound complications during the process of healing.…”