duminică, 25 iulie 2010
joi, 22 iulie 2010
marți, 20 iulie 2010
indulcitorii cu valoare calorica redusa . . . sunt ok
Br J Nutr. 2010 Jul 12:1-6. [Epub ahead of print]
Sweet-taste receptors, low-energy sweeteners, glucose absorption and insulin release.
Renwick AG, Molinary SV.
School of Medicine, University of Southampton, Southampton SO17 1BJ, UK.
Abstract
The present review explores the interactions between sweeteners and enteroendocrine cells, and consequences for glucose absorption and insulin release. A combination of in vitro, in situ, molecular biology and clinical studies has formed the basis of our knowledge about the taste receptor proteins in the glucose-sensing enteroendocrine cells and the secretion of incretins by these cells. Low-energy (intense) sweeteners have been used as tools to define the role of intestinal sweet-taste receptors in glucose absorption. Recent studies using animal and human cell lines and knockout mice have shown that low-energy sweeteners can stimulate intestinal enteroendocrine cells to release glucagon-like peptide-1 and glucose-dependent insulinotropic peptide. These studies have given rise to major speculations that the ingestion of food and beverages containing low-energy sweeteners may act via these intestinal mechanisms to increase obesity and the metabolic syndrome due to a loss of equilibrium between taste receptor activation, nutrient assimilation and appetite. However, data from numerous publications on the effects of low-energy sweeteners on appetite, insulin and glucose levels, food intake and body weight have shown that there is no consistent evidence that low-energy sweeteners increase appetite or subsequent food intake, cause insulin release or affect blood pressure in normal subjects. Thus, the data from extensive in vivo studies in human subjects show that low-energy sweeteners do not have any of the adverse effects predicted by in vitro, in situ or knockout studies in animals.
Sweet-taste receptors, low-energy sweeteners, glucose absorption and insulin release.
Renwick AG, Molinary SV.
School of Medicine, University of Southampton, Southampton SO17 1BJ, UK.
Abstract
The present review explores the interactions between sweeteners and enteroendocrine cells, and consequences for glucose absorption and insulin release. A combination of in vitro, in situ, molecular biology and clinical studies has formed the basis of our knowledge about the taste receptor proteins in the glucose-sensing enteroendocrine cells and the secretion of incretins by these cells. Low-energy (intense) sweeteners have been used as tools to define the role of intestinal sweet-taste receptors in glucose absorption. Recent studies using animal and human cell lines and knockout mice have shown that low-energy sweeteners can stimulate intestinal enteroendocrine cells to release glucagon-like peptide-1 and glucose-dependent insulinotropic peptide. These studies have given rise to major speculations that the ingestion of food and beverages containing low-energy sweeteners may act via these intestinal mechanisms to increase obesity and the metabolic syndrome due to a loss of equilibrium between taste receptor activation, nutrient assimilation and appetite. However, data from numerous publications on the effects of low-energy sweeteners on appetite, insulin and glucose levels, food intake and body weight have shown that there is no consistent evidence that low-energy sweeteners increase appetite or subsequent food intake, cause insulin release or affect blood pressure in normal subjects. Thus, the data from extensive in vivo studies in human subjects show that low-energy sweeteners do not have any of the adverse effects predicted by in vitro, in situ or knockout studies in animals.
miercuri, 14 iulie 2010
Martin Berkhan Protein Muffins
Protein muffins. Check out the stats on these bastards.
411 kcal
69 g protein
8.8 g fat
19 g carbs
Lots of protein. Ain't bad considering they're supposed to be pretty tasty. By popular demand, here's the recipe:
One whole extra large egg
The egg white from two extra large eggs
250 g low fat cottage cheese
33 g casein protein powder. Chocolate flavored powder was used for these.
One teaspoon bicarbonate
One teaspoon flax seed
Cinnamon
Sweetener. 1/2 deciliter, aspartame (Hermesetas). Not the liquid variety. You'll have to play this by ear depending on what sweetener you're using and how sweet you want them to be.
Mix everything together, split it up those muffin-shaped forms, and put it in the oven for 25 minutes at 150 degrees. There you go. Hope I got it right because I can't bake for shit. That's probably a good thing. Otherwise I'd be making cheesecakes all day long.
411 kcal
69 g protein
8.8 g fat
19 g carbs
Lots of protein. Ain't bad considering they're supposed to be pretty tasty. By popular demand, here's the recipe:
One whole extra large egg
The egg white from two extra large eggs
250 g low fat cottage cheese
33 g casein protein powder. Chocolate flavored powder was used for these.
One teaspoon bicarbonate
One teaspoon flax seed
Cinnamon
Sweetener. 1/2 deciliter, aspartame (Hermesetas). Not the liquid variety. You'll have to play this by ear depending on what sweetener you're using and how sweet you want them to be.
Mix everything together, split it up those muffin-shaped forms, and put it in the oven for 25 minutes at 150 degrees. There you go. Hope I got it right because I can't bake for shit. That's probably a good thing. Otherwise I'd be making cheesecakes all day long.
luni, 12 iulie 2010
joi, 8 iulie 2010
miercuri, 7 iulie 2010
marți, 6 iulie 2010
luni, 5 iulie 2010
low carb metabolic advantage...not really
e interesanta schimbarea de pozitie a autorului unui studiu care afirma in 2006 existenta unui avantaj metabolic al dietelor low carb (chiar keto)...aici
"Thus, the primary reason why low-carbohydrate diets tend to show superior weight loss in the short-term has nothing to do with a metabolic advantage, or an effect on insulin, or some other magical unknown effect. It all has to do with appetite control. When people consume a low-carbohydrate, high-protein diet, they are getting a “double-whammy” in regards to appetite regulation. They’re getting the dramatic benefit of increasing protein, and an additional (although smaller) benefit of a ketogenic diet. The bottom line is that the people on these diets spontaneously eat less….A LOT less.
The bottom line is that there is no metabolic advantage to a low carbohydrate intake that is independent of a high protein intake. There is a metabolic advantage to a high protein diet, which will increase the calories you burn by 80-100 calories per day. There is also a dramatic satiety advantage to a high protein intake. A low carbohydrate intake (low enough to cause ketosis) can increase this satiety advantage, but individual responses will vary. The best dietary approach for you will depend upon a variety of factors."
"Thus, the primary reason why low-carbohydrate diets tend to show superior weight loss in the short-term has nothing to do with a metabolic advantage, or an effect on insulin, or some other magical unknown effect. It all has to do with appetite control. When people consume a low-carbohydrate, high-protein diet, they are getting a “double-whammy” in regards to appetite regulation. They’re getting the dramatic benefit of increasing protein, and an additional (although smaller) benefit of a ketogenic diet. The bottom line is that the people on these diets spontaneously eat less….A LOT less.
The bottom line is that there is no metabolic advantage to a low carbohydrate intake that is independent of a high protein intake. There is a metabolic advantage to a high protein diet, which will increase the calories you burn by 80-100 calories per day. There is also a dramatic satiety advantage to a high protein intake. A low carbohydrate intake (low enough to cause ketosis) can increase this satiety advantage, but individual responses will vary. The best dietary approach for you will depend upon a variety of factors."
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