Dietary sodium restriction prevents kidney damage in high fructose fed rats The overall finding is: Sodium

depletion has a protective effect on target organ damage in hypertension independent of blood pressure. Metabolic Syndrome a cluster of cardiovascular risk factors including hypertension, type II diabetes, obesity, and dyslipidemia. These all lead to atherosclerotic cardiovascular disease. The link between all these cardiovascular risk factors is insulin resistance. Fructose leads to metabolic syndrome. Metabolic syndrome leads to renal damage. Long-term exposure to high fructose consumption is associated with protein urea, kidney enlargement, and focal tubulointerstitial injury and glomerulosclerosis. Evidence is accumulating that shows that immunological and inflammatory mechanisms have a role in the development and progression of kidney disease. Tumor necrosis factor alpha and interleukin six are relevant mediators that regulate inflammatory immune responses in diabetic nephropathy. There is evidence suggesting that insulin resistance may result from an inflammatory disorder, in which macrophages in adipose tissue and elsewhere may have an important role. Along with inflammation, oxidative stress seems to be implicated in renal injury in obesity and hypertension as well as in type II diabetic nephropathy in mice and in fructose fed rats. Some studies are showing a relationship between sugar consumption and sodium intake on renal sodium handling. Fructose appears to cause higher blood pressure in individuals with high sodium consumption as well as in spontaneously hypertensive rats fed a high sodium diet. Conversely, a low-sodium diet prevented changes in blood pressure induced by high dietary sucrose or fructose. Rationale: the effects of dietary sodium restriction on functional and morphological modifications of the kidney associated with insulin resistance have not yet been explored Objective: to evaluate the putative beneficial influence of a drastic reduction in sodium intake on fructose induced renal alterations. So basically, we know that metabolic syndrome leads to insulin resistance and we know that insulin resistance leads to both functional and morphological modifications of the kidney. The researchers hypothesized that sodium restriction was related to a reduction in the inflammatory and oxidative stress responses to high fructose induced insulin resistance in rats. The podocyte is a key cell type involved in the initial development of albuminuria. They therefore examined renal

ultrastructure in fructose fed rats. They then evaluated the influence of sodium restriction on retroperitoneal adipose tissue which may have a role in the development of insulin resistance. -------------------------------------Metabolic Syndrome is a constellation risk factors such as obesity, hypertension, type II diabetes, dyslipidemia, and cardiovascular disease in the presence of insulin resistance. Kidney disease (nephropathy) is associated with inflammation and oxidative stress, particularly in situations of obesity, hypertension, and type II diabetes; three conditions closely related to Metabolic Syndrome and Insulin Resistance. There is evidence that insulin resistance may result from an inflammatory disorder. Research has found a greater risk of microalbuminurea (a sign of kidney malfunction) in subjects with Metabolic Syndrome. High Fructose consumption has long been used as a method for inducing insulin resistance in rodents. Fructose consumption has also been associated with renal dysfunction in rats. Metabolic syndrome connects to hypertension, type II diabetes, obesity, and dyslipidemia these all connect to insulin resistance 1-3 Fructose is connected to obesity and metabolic syndrome. 4 5,6 Metabolic syndrome connects with renal damages. In humans, there is greater risk of chronic kidney disease and microalbuminuria in patients with metabolic syndrome.7 . Fructose fed rats show signs of renal dysfunction associated with renal hypertrophy, afferent arterialopathy, glomerular hypertension, renal vasoconstriction, and nephropathic changes compared with cornstarch fed rats. 8 Greater than six months exposure to high fructose consumption connects with proteinuria, kidney enlargement, and focal tubulointerstitial injury and glomerulosclerosis. 9,10 Immunological and inflammatory mechanisms connect with the development and progression of damages in chronic kidney diseases. TNF alpha and interleukin six are relevant mediators that regulate inflammatory immune responses in diabetic nephropathy. 11 insulin resistance may result from an inflammatory disorder mediated by macrophages in adipose tissue and elsewhere.12.

In obesity, hypertension (13), and type II diabetic nephropathy in mice and fructose fed rats, inflammation and oxidative stress connect with renal injury. 5,14 Sugar consumption also connects to sodium intake and renal sodium handling. Fructose connects with high blood pressure in individuals with high sodium consumption as well as spontaneously hypertensive rats. 15, 16. A low sodium diet prevents changes in blood pressure induced by high dietary sucrose (17) or fructose(16). Sodium withdrawal from diet connects with decreased cardiovascular and renal damage in angiotensin II hypertension. This is independent of arterial pressure reduction and possibly related to attenuation of the pro-oxidant effects of the peptide. 18 Rationale: the effects of dietary sodium restriction on functional and morphological modifications of the kidney associated with insulin resistance have not yet been explored. Objective: to evaluate the putative beneficial influence of a drastic reduction in sodium intake on fructose induced renal alterations. They tested the hypothesis that sodium restriction was related to a reduction in the inflammatory and oxidative stress responses to high fructose induced insulin resistance in rats. The podocyte is a key cell type involved in the initial development of albuminuria, particularly in obesity or type II diabetes, renal ultrastructure was examined in fructose fed rats. Finally, they evaluated the influence of sodium restriction on retroperitoneal adipose tissue, which may have a role in the development of insulin resistance. 20