[A.Steinbach]

Ursprungligen postat av mikaelj

Det här är vad jag har fått förklarat för mig:

Insulin får LPL att sätta sig på fettcellerna istället för muskelcellerna, vilket gör det svårt för muskelcellerna att använda fett som bränsle. Socker i fettcellerna binder upp fett.

Helt kort, minimera det insulinberoende glukosupptaget i fettväv och därmed minimera bildningen av glycerolskelett för TAG-syntes. Utan glycerol-3-fosfat -- ingen TAG-syntes i fettväven.

Lipoprotein lipase (EC 3.1.1.34; LPL) is a key enzyme regulating the disposal of lipid fuels in the body. It is expressed in a number of peripheral tissues including adipose tissue, skeletal and cardiac muscle and mammary gland. Its role is to hydrolyse triacylglycerol (TG) circulating in the TG-rich lipoprotein particles in order to deliver fatty acids to the tissue. It appears to act preferentially on chylomicron-TG, and therefore may play a particularly important role in regulating the disposition of dietary fatty acids. LPL activity is regulated according to nutritional state in a tissue-specific manner according to the needs of the tissue for fatty acids. For instance, it is highly active in lactating mammary gland; in white adipose tissue it is activated in the fed state and suppressed during fasting, whereas the reverse is true in muscle. Such observations have led to the view of LPL as a metabolic gatekeeper, especially for dietary fatty acids. However, closer inspection of its action in white adipose tissue reveals that this picture is only partially true. Normal fat deposition in adipose tissue can occur in the complete absence of LPL, and conversely, if LPL activity is increased by pharmacological means, increased fat storage does not necessarily follow. LPL appears to act as one member of a series of metabolic steps which are
regulated in a highly coordinated manner. In white adipose tissue, it is clear that there is a major locus of control of fatty acid disposition downstream from LPL. This involves regulation of the pathway of fatty acid uptake and esterification, and appears to be regulated by a number of factors including insulin, acylation-stimulating protein and possibly leptin.

Lipoprotein lipase and the disposition of dietary fatty acids
British Journal of Nutrition (1998), 80, 495–502

We have studied the fate of lipoprotein lipase (LPL)-derived fatty acids by measuring arteriovenous differences across subcutaneous adipose tissue and skeletal muscle in vivo. Six subjects were fasted overnight and were then given 40 g of triacylglycerol either orally or as an intravenous infusion over 4 h. Intracellular lipolysis (hormone-sensitive lipase action; HSL) was suppressed after both oral and intravenous fat loads (P , 0.001). Insulin, a major regulator of HSL activity, showed little change after either oral or intravenous fat load, suggesting that suppression of HSL action occurred independently of insulin. The rate of action of LPL (measured as triacylglycerol extraction) increased with both oral and intravenous fat loads in adipose tissue (P 5 0.002) and skeletal muscle (P 5 0.001).

Effects of an oral and intravenous fat load on adipose tissue and forearm lipid metabolism
Am J Physiol Endocrinol Metab 276:241-248, 1999.

Acylation Stimulating Protein (ASP) is a small (mol wt 14,000), basic (PI 9.0) protein present in human plasma. When examined in vitro with normal human cultured skin fibroblasts and adipocytes, ASP appears to be the most potent stimulant of triglyceride synthesis yet described. In this study, a competitive ELISA assay for ASP has been developed using immunospecific polyclonal antibodies, and ASP levels have been measured in seven normal subjects. Following an oral fat load, a sustained significant increase in ASP occurs, whereas after an oral glucose load, ASP levels do not change significantly. These responses are entirely opposite to those of insulin, which rises sharply but transiently after an oral glucose load but is unchanged after an oral fat load. Both the fasting and peak ASP levels were significantly related to the postprandial lipemia. These data provide the first in vivo evidence that Acylation Stimulating Protein may play an important physiological role in the normal response to an oral fat load

Metabolic response of Acylation Stimulating Protein to an oral fat load
J Lipid Res. 1989. 30: 1727-1733.

Kroppen är anpassad för att kunna lagra energi/fett oavsett insulinnivå. Insulinnivån som är beroende av makronutrientfördelningen styr substratutnyttjandet inte fettbalansen.