Laxx
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Die Hauptursache von Insulinresistenz sind nicht KH sondern Fett. Das "böse" Körperfett führt dazu das die KH nicht richtig verarbeitet werden können.
Deswegen ist auch die erste Maßnahme bei T2D idR Abspecken. Low Carb kann sich eignen die Krankheit besser zu managen.
"The most effective site for storage of excess fat calories is the adipose tissue including those excess calories from carbohydrates that are converted to fat in the liver. [...] As long as those fat cells are healthy, there are no adverse metabolic effects (except excess weight) for the person. This is why approximately one-third of obese individuals fall into the category of “metabolically healthy obese” [44]. They have excess body fat but no metabolic disturbances that characterize the manifestation of insulin resistance.
However, fat cells do not have an unlimited capacity to expand. Even though the adipose tissue is highly vascularized, the over-expansion of existing fat cells can create hypoxia, which activates the HIF-1 gene [45, 46]. This results in the increased expression of both JNK and IKK thereby creating inflammation within the fat cell [47]. This inflammation, in turn, creates insulin resistance within the fat cell.
In the adipose tissue, insulin is normally an anti-lipolytic hormone as it decreases the activity of hormone-sensitive lipase (HSL), which is required to release stored fatty acids [48]. With the development of cellular inflammation and insulin resistance in the fat cell, higher levels of free fatty acids (FFA) can leave the fat cell to enter into the circulation and be taken up by other organs, such as the liver and the skeletal muscles that are unable to safely store large amounts of fat. As described later, this leads to developing insulin resistance in these organs."
Deswegen ist auch die erste Maßnahme bei T2D idR Abspecken. Low Carb kann sich eignen die Krankheit besser zu managen.
"The most effective site for storage of excess fat calories is the adipose tissue including those excess calories from carbohydrates that are converted to fat in the liver. [...] As long as those fat cells are healthy, there are no adverse metabolic effects (except excess weight) for the person. This is why approximately one-third of obese individuals fall into the category of “metabolically healthy obese” [44]. They have excess body fat but no metabolic disturbances that characterize the manifestation of insulin resistance.
However, fat cells do not have an unlimited capacity to expand. Even though the adipose tissue is highly vascularized, the over-expansion of existing fat cells can create hypoxia, which activates the HIF-1 gene [45, 46]. This results in the increased expression of both JNK and IKK thereby creating inflammation within the fat cell [47]. This inflammation, in turn, creates insulin resistance within the fat cell.
In the adipose tissue, insulin is normally an anti-lipolytic hormone as it decreases the activity of hormone-sensitive lipase (HSL), which is required to release stored fatty acids [48]. With the development of cellular inflammation and insulin resistance in the fat cell, higher levels of free fatty acids (FFA) can leave the fat cell to enter into the circulation and be taken up by other organs, such as the liver and the skeletal muscles that are unable to safely store large amounts of fat. As described later, this leads to developing insulin resistance in these organs."
Ja, das ist meine Meinung.Manche Beiträge von dir hören sich so an, als ob da viel Lärm um nichts gemacht würde
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