Esta revision permitira comprender la relacion entre el consumo de fructosa anadida a los alimentos en altas concentraciones y el riesgo de desarrollar obesidad, resistencia a la insulina,
lipogenesis de novo e inflamacion, danando la salud de la poblacion general.
Interplay between ChREBP and SREBP-1c coordinates postprandial glycolysis and
lipogenesis in livers of mice.
Some studies have shown that endoplasmic reticulum stress (ERS) signaling pathways contribute to the development of insulin resistance and hepatic steatosis in NAFLD.[9],[10],[11],[12] X-box binding protein-1 (XBP-1) is a major transcription regulator of the unfolded protein response (UPR), mediating adaptation to ERS.[13] Here, we hypothesized that XBP-1 plays a role in the process of fructose-stimulated
lipogenesis in HepG2 cells.
The effect of the latter is stimulation of SREBP-lc, which is central to sebaceous
lipogenesis, sebum fatty acid production, and monosaturation.
Effects of dietary fructose restriction on liver fat, de novo
lipogenesis, and insulin kinetics in children with obesity.
In the postdoctoral category, first was Vimal Ramachandran with the poster A microRNA-based strategy to combat hypercholesterolemia; and joint second were Murugan Subramanian with A microRNA-dependent pathway regulating ER stress-induced
lipogenesis via mTOR in liver; and Yasser Majeed with Functional interaction between Sirt1 deacetylase and Myc oncogene regulates adipogenesis.
These hormones, both alone and combined, can stimulate lipolysis or
lipogenesis in various types of adipose tissue (4).
Using western blotting, the HL group decreased the protein levels of Srebp1, Srebp2, and ABCA for hepatic
lipogenesis and increased the protein levels of PPARa, which mainly included fatty acid [beta]-oxidation and various lipid metabolisms of liver, compared with the HU group (Figure 4(a)).
Another important aspect of fatty acid metabolism disorders is the de novo
lipogenesis in the liver.
(c) RT-qPCR analysis for the genes related to fatty acid synthesis and
lipogenesis, fatty acid and lipid uptake, and [beta]-oxidation (n = 3).
This shows that GH and not IGF-1 directly affects lipid uptake and
lipogenesis [5].
Moreover, it can induce B-oxidation in the liver while decreasing the expression of sterol regulatory element-binding protein 1 (SREBP1) therefore inhibiting
lipogenesis. Leptin is a proinflammatory cytokine that acts through the leptin receptor (OBRb), activating the cyclic adenosine monophosphate--(cAMP-) dependent protein kinase A (PKA) extracellular signal-regulated kinase (ERK) 1/2 and p38 mitogen-activated protein kinase (MAPK) pathways [9].