Exogenous pathway for lipid metabolism:

Methods:Mice were pre-conditioned using either a diet containing the potent PPARA agonist Wy-14643 or an EODF regimen prior to acute fasting. Ppara-null mice were used to assess the contribution of PPARA activation during the metabolic response to EODF. Livers were collected for histological, biochemical, qRT-PCR, and Western blot analysis.

Endogenous pathway for lipid metabolism:

Explore the Overview of Lipid Metabolism from the Professional ..

Lipid metabolism is the synthesis and degradation of lipids in cells

Results:Acute fasting activated PPARA and led to steatosis, whereas EODF protected against fasting-induced hepatic steatosis without affecting PPARA signaling. In contrast, pretreatment with Wy-14,643 did activate PPARA signaling but did not ameliorate acute fasting-induced steatosis and unexpectedly promoted liver injury. Ppara ablation exacerbated acute fasting-induced hypoglycemia, hepatic steatosis, and liver injury in mice, whereas these detrimental effects were absent in response to EODF, which promoted PPARA-independent fatty acid metabolism and normalized serum lipids.

10 Lipid Metabolism | Lipoprotein | Biosynthesis

Objective:Brain insulin-induced improvement in glucose homeostasis has been proposed to be mediated by the parasympathetic nervous system. Non-invasive transcutaneous auricular vagus nerve stimulation (taVNS) activating afferent branches of the vagus nerve may prevent hyperglycemia in diabetes models. We examined the effects of 14-min taVNS vs sham stimulation by Cerbomed Nemos® on glucose metabolism, lipids, and hepatic energy homeostasis in fasted healthy humans (n = 10, age 51 ± 6 yrs, BMI 25.5 ± 2.7 kg/m2).

Lipid metabolism in the mammary gland or ruminant animals

Low HDL-cholesterol is a component of the metabolic syndrome that is characterized by obesity, insulin resistance, dyslipidemia, and hypertension

Overview of lipid metabolism ..

N2 - Hyperlipidemia in the nephrotic syndrome results from increased synthesis and decreased catabolism of lipoproteins. The contribution of each to establishing blood lipid levels is unknown. Increased triglyceride rich lipoprotein concentration, very low density lipoprotein (VLDL) and intermediate density lipoprotein (IDL) primarily results from decreased clearance. This defect is clue in part to reduced lipoprotein lipase (LPL) on the vascular endothelium resulting either from decreased synthesis or inadequate binding of this enzyme to endothelial surfaces. In contrast, both low density lipoprotein (LDL) and lipoprotein(a) [Lp(a)] concentrations are increased. Unlike the case of albumin or transferrin, or apoA-I in the rat, LDL apoB 100 synthesis is not related to that of albumin, suggesting a different mechanism of regulation or a response to a stimulus that is not the same as that augmenting the synthesis of nonlipoproteins. Evidence is presented for synthesis of LDL through a mechanism that bypasses the normal delipidation pathway that requires a VLDL precursor for LDL formation. HDL concentration is normal but maturation is impaired leading to a shift from the larger HDL2 to the smaller HDL3, a variant that is less effective as a transporter of the LPL cofactor apolipoprotein C II.

Overview of Lipid Metabolism in ..

Hyperlipidemia in the nephrotic syndrome results from increased synthesis and decreased catabolism of lipoproteins. The contribution of each to establishing blood lipid levels is unknown. Increased triglyceride rich lipoprotein concentration, very low density lipoprotein (VLDL) and intermediate density lipoprotein (IDL) primarily results from decreased clearance. This defect is clue in part to reduced lipoprotein lipase (LPL) on the vascular endothelium resulting either from decreased synthesis or inadequate binding of this enzyme to endothelial surfaces. In contrast, both low density lipoprotein (LDL) and lipoprotein(a) [Lp(a)] concentrations are increased. Unlike the case of albumin or transferrin, or apoA-I in the rat, LDL apoB 100 synthesis is not related to that of albumin, suggesting a different mechanism of regulation or a response to a stimulus that is not the same as that augmenting the synthesis of nonlipoproteins. Evidence is presented for synthesis of LDL through a mechanism that bypasses the normal delipidation pathway that requires a VLDL precursor for LDL formation. HDL concentration is normal but maturation is impaired leading to a shift from the larger HDL2 to the smaller HDL3, a variant that is less effective as a transporter of the LPL cofactor apolipoprotein C II.