Although for some a high-fat, high-protein diet can lead to weight loss and blood sugar normalization, other research points to ways it can worsen either condition, based on the body’s reaction to the foods.
A specific protein activated in the body called Bcl10 triggers inflammatory marker NF-kB when it reacts to a certain fat (in this case, palmitate), and sets up a cascade of conditions that can make weight gain more harmful and the body more prone to insulin resistance.
Certainly, heavily processed foods with a high-fat content can lead to a larger waistline and increased risk of diabetes, so it’s important to approach any dietary advice with careful attention to what works best for you, and you’re entire regimen of exercise, sleep, stress, and overall food intake. It’s also easy to forget that these foods also damage the liver, one of the aspects of insulin resistance examined by this study.
If anything, this study points to a common sense outlook when it comes to eating: fruits and vegetables are still important, and healthy fats – as opposed to omega-6 heavy refined oils and deep-fried foods – are a must for avoiding weight gain and high blood sugar levels.
Van Beek M, Oravecz-Wilson KI, Delekta PC, et al. Bcl10 Links Saturated Fat Overnutrition with Hepatocellular NF-κB Activation and Insulin Resistance. Cell reports. 2012;1(5):444-452.
Excess serum free fatty acids (FFAs) are fundamental to the pathogenesis of insulin resistance. With high-fat feeding, FFAs activate NF-kB in target tissues, initiating negative crosstalk with insulin signaling. However, the mechanisms underlying FFA-dependent NF-kB activation remain unclear. Here, we demonstrate that the saturated FA, palmitate, requires Bcl10 for NF-kB activation in hepatocytes. Uptake of palmitate, metabolism to diacylglycerol, and subsequent activation of protein kinase C (PKC) appear to mechanistically link palmitate with Bcl10, known as a central component of a signaling complex that, along with CARMA3 and MALT1, activates NF-kB downstream of selected cell surface receptors. Consequently, Bcl10-deficient mice are protected from hepatic NF-kB activation and insulin resistance following brief high-fat diet, suggesting that Bcl10 plays a major role in the metabolic consequences of acute overnutrition. Surprisingly, while CARMA3 also participates in the palmitate response, MALT1 is completely dispensable, thereby revealing an apparent nonclassical role for Bcl10 in NF-kB signaling.
Link to complete study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3375919/
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