Comment - Ok, we know that transfats are bad for you! They are unnatural oxidise easily and throw of free radicals which do you no good at all.
So just to make sure we know how bad they are, they fed some to the monkeys! It made them fat and increased their insulin resistance, putting them on the road to diabetes.
We need to stick to good, safe fats. Contrary to popular opinion that means saturated fat. Saturated fats are stable. Fats are attacked by oxygen. Just like iron left out in the rain, fats oxydise (rust). But oxygen can only attack fats where there are double bonds. This is why saturated fats don't spoil but polyunsaturated margarines must be kept in the fridge. And the more double bonds a fatty acid has, the more it oxydises and the more ' free radicals ' it throws off. Check out the Chemistry here.
Trans fat diet induces abdominal obesity and changes in insulin sensitivity in monkeys.
OBJECTIVE: There is conflicting evidence about the propensity of trans fatty acids (TFAs) to cause obesity and insulin resistance. The effect of moderately high intake of dietary monounsaturated TFAs on body composition and indices of glucose metabolism was evaluated to determine any pro-diabetic effect in the absence of weight gain. RESEARCH METHODS AND PROCEDURES: Male African green monkeys (Chlorocebus aethiops; n=42) were assigned to diets containing either cis-monounsaturated fatty acids or an equivalent diet containing the trans-isomers (approximately 8% of energy) for 6 years. Total calories were supplied to provide maintenance energy requirements and were intended to not promote weight gain. Longitudinal body weight and abdominal fat distribution by computed tomography scan analysis at 6 years of study are reported. Fasting plasma insulin, glucose, and fructosamine concentrations were measured. Postprandial insulin and glucose concentrations, and insulin-stimulated serine/threonine protein kinase (Akt), insulin receptor activation, and tumor necrosis factor-alpha concentrations in subcutaneous fat and muscle were measured in subsets of animals. RESULTS: TFA-fed monkeys gained significant weight with increased intra-abdominal fat deposition. Impaired glucose disposal was implied by significant postprandial hyperinsulinemia, elevated fructosamine, and trends toward higher glucose concentrations. Significant reduction in muscle Akt phosphorylation from the TFA-fed monkeys suggested a mechanism for these changes in carbohydrate metabolism. DISCUSSION: Under controlled feeding conditions, long-term TFA consumption was an independent factor in weight gain. TFAs enhanced intra-abdominal deposition of fat, even in the absence of caloric excess, and were associated with insulin resistance, with evidence that there is impaired post-insulin receptor binding signal transduction.
So just to make sure we know how bad they are, they fed some to the monkeys! It made them fat and increased their insulin resistance, putting them on the road to diabetes.
We need to stick to good, safe fats. Contrary to popular opinion that means saturated fat. Saturated fats are stable. Fats are attacked by oxygen. Just like iron left out in the rain, fats oxydise (rust). But oxygen can only attack fats where there are double bonds. This is why saturated fats don't spoil but polyunsaturated margarines must be kept in the fridge. And the more double bonds a fatty acid has, the more it oxydises and the more ' free radicals ' it throws off. Check out the Chemistry here.
Trans fat diet induces abdominal obesity and changes in insulin sensitivity in monkeys.
OBJECTIVE: There is conflicting evidence about the propensity of trans fatty acids (TFAs) to cause obesity and insulin resistance. The effect of moderately high intake of dietary monounsaturated TFAs on body composition and indices of glucose metabolism was evaluated to determine any pro-diabetic effect in the absence of weight gain. RESEARCH METHODS AND PROCEDURES: Male African green monkeys (Chlorocebus aethiops; n=42) were assigned to diets containing either cis-monounsaturated fatty acids or an equivalent diet containing the trans-isomers (approximately 8% of energy) for 6 years. Total calories were supplied to provide maintenance energy requirements and were intended to not promote weight gain. Longitudinal body weight and abdominal fat distribution by computed tomography scan analysis at 6 years of study are reported. Fasting plasma insulin, glucose, and fructosamine concentrations were measured. Postprandial insulin and glucose concentrations, and insulin-stimulated serine/threonine protein kinase (Akt), insulin receptor activation, and tumor necrosis factor-alpha concentrations in subcutaneous fat and muscle were measured in subsets of animals. RESULTS: TFA-fed monkeys gained significant weight with increased intra-abdominal fat deposition. Impaired glucose disposal was implied by significant postprandial hyperinsulinemia, elevated fructosamine, and trends toward higher glucose concentrations. Significant reduction in muscle Akt phosphorylation from the TFA-fed monkeys suggested a mechanism for these changes in carbohydrate metabolism. DISCUSSION: Under controlled feeding conditions, long-term TFA consumption was an independent factor in weight gain. TFAs enhanced intra-abdominal deposition of fat, even in the absence of caloric excess, and were associated with insulin resistance, with evidence that there is impaired post-insulin receptor binding signal transduction.
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