Relationship between Adiposity, inulin resistance and gout.

Relationship between Adiposity, inulin resistance and gout.

• 1.
  ADIPOSITY, INSULIN RESISTANCE ANDGOUT
• 2.
  ADIPOSITY AND GOUT Obesity –excessive accumulation of body fat(adipose tissue)  Obesity is associated with a state of chronic low grade inflammation that contributes to insulin resistance, type 2 diabetes and increased risk of hyperuricemia and gout.  Inflammatory cells accumulate in adipose tissue with increasing body weight and evidence in mounting that implicates this inflammatory cell as significant contributors to obesity associated insulin resistance.  Although the pathogenesis of insulin resistance in obesity Is multifactorial, there is evidence that adipose tissue macrophages with chronic, low grade inflammation are a major contributor.  Furthermore, many regulators play a critical role in obesity by regulating macrophage recruitment such as c-cmotit chemokine receptor 5 (CCRS); phosphoinositide-3-kinase, dendritic cells, and adipose tissue size.
• 3.
   Inflammatory mediatorsin adipose tissue has been shown to cause insulin resistance in adipocytes e.g. TNF-α treated adipocytes exhibited decreased insulin signaling and subsequently decreased glucose up take.  It is suggested that insulin resistance may be a mediator between adiposity and hyperuricemia (gout) as insulin excretion may be exacerbated by adipocytes and insulin has been identified as cause of hyperuricemia by exhibiting uric acid formation.
• 4.
  INSULINE RESISTANCE ANDGOUT.  Hyperuricemia and metabolic syndrome.  metabolic syndrome is currently defined as having at least 3-5 signs (abdominal obesity, impaired fasting glucose, hypertriglyceridemia, low HDL cholesterol and elevated blood pressure.  In patients with manifest atherosclerosis, both presence of more than 3 metabolic risk factors and the presence of high waist circumference are associated risk of type 2 diabetes.
• 5.
  Case studies…  Insome case series studies, it reported that prevalence of metabolic syndrome high with patients with gout. Hyperuricemia has been associated with metabolic syndrome in studies of both healthy individuals and patients may also precipitate cardiovascular diseases of which metabolic syndrome is a strong risk factor.  The most difference in the prevalence of hyperuricemia was found in male adults with metabolic syndrome, compared with those with none metabolic syndrome.
• 6.
   Higher prevalenceof metabolic syndrome was also found in men with hyperuricemia. Even in those with normal uricemia, higher serum uric acid levels were associated with metabolic syndrome.  In those with normal BMI, the prevalence of metabolic syndrome was more than 10 fold higher in those with uric acid levels of 10 mg/dl or greater compared with uric acid levels less than 5 mg/dl.  Thus, all data shows us that, those with hyperuricemia are always cormorbidited with metabolic syndrome.
• 7.
   Elevated meanserum uric acid levels were found to be significantly increase by the component numbers of metabolic syndrome and further more, the prevalence of metabolic syndrome also increased significantly with uric acid levels.  Higher uric acid levels are associated with metabolic syndrome and the converse is true that patients with hyperuricemia frequently have metabolic syndrome. It was therefore suggested that, insulin resistance is the pathophysiology mechanism for the association
• 8.
  Metabolic syndrome withinsulin resistance  The abnormal components of metabolic syndrome usually cogent conceptual pathogen to reflect the essential cause. However, insulin resistane is a common feature of patients with abnormal metabolic components.  Insulin secreted by pancreatic beta cells cause the cells to take up glucose from blood and when the cells have a reduced sensitivity to stimulation of glucose uptake or insulin in the face of normal or raised glucose concentration, the situation is defined as insulin resistance.
• 9.
   If insulinresistance exits, more insulin needs to be secreted by the pancreas with resultant compensatory hyperinsulinemia.  The result is glucose intolerance and hyperglycemia and subsequently type-2 diabetes. In addition, hyperinsulinemia may aggravate insulin resistance by interfering with insulin signaling pathways and further excavating insulin resistance
• 10.
  Continued…  Insulin resistanceis thought to be an important correlate of other risk factors of metabolic syndrome such as dyslipidemia and hypertension.  Patients with essential hypertension were found to be associated with insulin resistance and even among the normotensive population. Insulin resistance is shown to be associated with high blood pressure levels.
• 11.
   Insulin hasa direct effect in the dilation of peripheral vasculature.  Hyperinsulinemia could lead to hypertension by activating renin-angiotensin system and subsequently to decrease renal blood flow, increased urate re-absorption and xanthine oxidase production resulting in hyperuricemia, As urate concentration increases in physiologic fluids, the risk for supersaturation and crystal formation generally increases hence gout.
• 12.
  Conclusion of therelationship between adiposity, insulin resistance and gout. Adiposity insulin resistance hyperinsulinemia,  hyperuricemia inhibition of urate excretion  GOUT  Adiposity leads to insulin resistance which leads to hyperinsulinemia, leading to inhibition of excretion urate by the kidney leading to hyperuricemia, hence gout.