Etiquetado: fructosa

Grasa dietaria y grasa corporal

He preparado este esquema como parte de una futura entrada del blog. Como me parece interesante, lo publico por anticipado:


Algunas citas:

Hepatic VLDL production is primarily substrate driven, the most important regulatory substrate being fatty acids. Fatty acids may be derived from at least four sources: (1) de-novo lipogenesis, (2) cytoplasmic triglyceride stores, (3) fatty acids derived from lipoproteins taken up directly by the liver, or (4) exogenous fatty acids (plasma free fatty acids). (fuente)

our observations indicate that hepatic insulin sensitivity is regulated by short-term changes in the intake of simple sugars, but not of fat. This was observed at very high, hypercaloric intakes for both fructose and glucose. (fuente)

A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride (TG) synthesis, driven by the high flux of glycerol and acyl portions of TG molecules from fructose catabolism. These metabolic disturbances appear to underlie the induction of insulin resistance commonly observed with high fructose feeding in both humans and animal models (fuente)

insulin at concentrations that are within the normal physiological range lowers blood glucose through inhibiting hepatic glucose production (fuente)

insulin can regulate the uptake of LCFA by tissues via FATP1 activation and that FATPs determine the tissue distribution of dietary lipids (fuente)

Lipoprotein lipase (LPL), located on the capillary endothelium of extrahepatic tissues, catalizes the rate-limiting step in the hydrolysis of triglycerides (TGs) from circulating chylomicrons and very low density lipoprotein (fuente)

Lipoprotein lipase (LPL) in the capillaries of adipose tissue hydrolyses circulating TG, mainly the dietary fat carried in the chylomicrons (fuente)

in the absence of LPL (as in genetic mutations) there is a complete absence of chylomicron hydrolysis (fuente).

Insulin up-regulates adipose tissue expression of LPL, through multiple mechanisms (fuente)

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