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. 2019 Feb 3;11(2):332. doi: 10.3390/nu11020332

Figure 4.

Figure 4

Proposed mechanism of the carob fruit extract (CFE) effects on lipoprotein metabolism. The diabetogenic status induced by STZ-NAD administration in addition to the atherogenic diet give raise to a hyperglycemic status compatible with a decrease in plasma insulin levels [25]. The insulinemia reduction implies higher FFA release increased VLDL production and Ldlr decrease [6]. The cholesterol-enriched diet produces increased level of cholesterol-enriched VLDL (β-VLDL) [9,13]. Green arrow indicates the increase (↑) or decrease (↓) for each marker assigned. Stages: (1) CFE increases the fat excretion of the atherogenic diet, mainly by decreasing dietary digestibility (reduction of fat digestion and absorption); (2) the lower plasma cholesterol and triglycerides in CFE groups correspond to a lower production of triglyceride enriched-VLDL and decreased β-VLDL synthesis; (3) CFE decreases the IDL and LDL levels, as a consequence of a higher hepatic Ldlr levels; (4) CFE increases the plasma and liver AE activities, reducing the VLDL and liver oxidation observed in the non-CFE rats. AE, arylesterase; CFE, carob fruit extract; FFA, free fatty acids; HDL, high-density lipoproteins; HL, hepatic lipase; HSL, hormone-sensitive lipase; IDL, intermediate-density lipoproteins; LDL, low-density lipoproteins; Ldlr, low density lipoprotein receptor; LRP, low density lipoprotein receptor-related protein; QM, chylomicrons; QMr, remnant chylomicrons; SR-B1, hepatic scavenger receptor B-I; VLDL, very low-density lipoproteins; β-VLDL, cholesterol-enriched very low-density lipoproteins.