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Thiazolidinediones have been shown to decrease UAE in diabetics and the reduction in UAE has been associated with the thiazolidinediones-induced increase in serum adiponectin levels ( Miyazaki et al . 2007 ). These findings indicate that the beneficial effects of thiazolidinediones on diabetic nephropathy may be mediated by the thiazolidinediones-induced upregulation of circulating adiponectin which is PPARγ-dependent. Consistently, elevated serum adiponectin levels in PPARγ-agonist treated mice appear to increase recovery of injured podocytes ( Rutkowski et al . 2013 ).

Fenofibrate treatment decreases UAE, but the exact underlying mechanism remains unknown ( Keech et al . 2005 ). Moreover, fenofibrate has been reported to increase adiponectin expression in adipose tissue and serum adiponectin levels through PPARα activation and HDL elevation ( Nike VAPOR STREET FLYKNIT SNEAKERS wt0ahJk6e6
). Thus, the fenofibrate-induced elevation of serum adiponectin levels may contribute to the concomitant decrease in UAE, because of the renoprotective effects of adiponectin. Consistently, unpublished data from a previous trial performed by our study group showed that the percentage change in circulating HMW adiponectin over 3 months of fenofibrate treatment was negatively correlated with the percentage change in urinary albumin to creatinine ratio (ACR) ( r =−0.648, P =0.043) ( Nike SB PORTMORE Slipons white/light bone VeQ7MS

Weight loss can induce a decrease in UAE in overweight or obese subjects ( Kiortsis Christou 2012 ). Long-term diets have been shown to increase serum adiponectin levels ( Christou Kiortsis 2013 ), indicating a possible role of adiponectin on mediating, at least in part, the weight loss-induced changes of UAE. There is a study mentioning that the change in serum adiponectin levels over 1 year of diet was not significantly correlated with the change in ACR ( Nakatsuji et al . 2010 ). Unpublished data from a previous trial performed by our study group showed that circulating HMW adiponectin at baseline was negatively correlated with the percentage change of logACR over 3 months of diet ( r =−0.769, P =0.003) ( Christou et al . 2012 ). Thus, high baseline serum adiponectin levels may predict a more favourable response of UAE during diet, possibly reflecting a higher grade of nephroprotection. Further studies are needed to elucidate the possible role of adiponectin in the weight-loss-induced decrease in UAE.

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Adiponectin is an adipokine that appears to have renoprotective effects through AMPK-activated pathways, resulting in the prevention of albuminuria. The relationship between circulating adiponectin and albuminuria has been reported to show a biphasic pattern. A negative relationship exists in the case of normoalbuminuria, possibly reflecting the increased renal clearance of adiponectin together with the renoprotective effects of adiponectin, and a positive association in more advanced albuminuria, indicating the counteracting upregulation of serum adiponectin levels to mitigate renal injury. Taking into account the fact that the currently believed route of renal biodegradation/excretion of adiponectin is not based on firm evidence, the confirmation of this route and the exploration of the exact related pathways are prerequisites for understanding the role of adiponectin with regard to renal physiology. In addition, the accepted renoprotective role of adiponectin has been based almost exclusively on data from nonhuman experiments, necessitating the performance of studies investigating the relevant issues in human experimental settings. Further clinical studies are needed to translate convincing experimental evidence for the nephroprotective role of adiponectin into clinical practice that could create new therapies for albuminuria, targeting specific pathways of adiponectin action.

The Nourished Life

How to Eat Well, Live Healthy and Love Life with More Balance and Less Stress

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For years we’ve been told to avoid butter and instead use vegetable oils as our primary fat source. Mainstream science claims this will save our hearts. But industrial oils like soybean, corn and canola oil are hiding a dirty little secret: consuming them could very well increase your risk of cancer.

What Are Polyunsaturated Fats?

Saturated fats have no double bonds (like those in coconut oil ) and monounsaturated fats (like those in olive oil) have one double bond. However, polyunsaturated fats (also known as PUFAs for short) are linked by multiple double bonds . This is what makes polyunsaturated oils highly unstable and fare more vulnerable to oxidation than other fats. Bruce Fife offers an excellent explanation of the different kinds of fats and how they affect our health is his book The Coconut Oil Miracle .

The Cancer Connection

Many experts now acknowledge that refined polyunsaturated oils are damaged fats and should be avoided. This leads to the assumption that cold-pressed organic oils are inherently acceptable because they are less refined. However, even gently processed polyunsaturated oils are unstable, and oxidation can still occur once these fats are in the body. And oxidation is linked to cancer and other degenerative diseases.

In addition to the dangers of oxidation, there are also bonafide concerns about the omega-6 content of polyunsaturated oils. A recent San Francisco study demonstrated that under laboratory conditions, omega-6 fatty acids could accelerate the growth of prostate tumor cells.

Other studies show that improving the omega-3 to omega-6 ratio can lower the risk of certain cancers. Experts vary in their specific ratio recommendations, but most suggest a ratio of between 1:1 and 1:4 at most . The average modern diet has an omega-3 to omega-6 ratio of 1:20 (or more!).

The blame for this imbalance can be squarely placed on the rapid increase of vegetable oils in our diets during the past century:

While some vegetable oils do contain small amounts of omega-3 fatty acids, for the most part they consist of omega-6. Eating more vegetable oils does nothing to correct the imbalance of omega 3 to omega 6 fatty acids in our diet.

To combat this effect, the typical recommendation is to increase omega-3 consumption. That’s kind like bailing water out of a sinking ship with a baseball cap. This problem is far more effectively resolved by reducing omega-6 intake. Eliminating or drastically decreasing polyunsaturated oil consumption is the best way to do this.

How to Decrease Your Polyunsaturated Fat Intake

Here’s how you can cut excess PUFAs from your diet:



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