Figure 4

Effect of AM-HM on messengers of hepatic insulin signaling cascade-Akt, signal transducer and activator of transcription 3 (p-tyr-STAT-3), c-Jun N-terminal kinase (JNK1/2), 5′ AMP-activated protein kinase (AMPK-1α), Forkhead box protein O1 (FoxO1), sterol regulatory element-binding protein 1c (SREB1c). In study I, the Akt levels were significantly raised in 4FDR and 4AMR implying activation of insulin mediated glycolysis and glycogenesis pathways to siphon fructose. In study II, the unaltered levels of Akt in 8FDR, is suggestive of defect in insulin downstream signaling. In 8AMR, the downstream signaling sensitivity was significantly restored which coordinated with reduced insulin levels. The STAT-3 levels were significantly raised in 4AMR as compared to 4FDR. Chronic fructose ingestion significantly raised STAT-3 levels in 8 FDR as compared to 8NDR. At adulthood, 8AMR recorded significant reduction of STAT-3 as compared to 8FDR. The negative regulator of insulin signaling cascade, JNK, was significantly raised in 4FDR but reduced in 4AMR. At adulthood, the JNK level was not significantly different in 8FDR from 8NDR. The AMPK activity was significantly raised in 4AMR, that is indicative of fructose-induced ATP depleted state that was reversed in 4AMR but not in 8AMR. The 4AMR and 8AMR recorded significantly reduced FoxO1 levels as compared to 4FDR and 8FDR, respectively. The level of SREBP-1c were significantly reduced in 4FDR in consonance with reduced total cholesterol level. Chronic fructose ingestion, significantly reduced SREBP-1c levels in 8FDR as compared to 8NDR that was also reflected in total cholesterol levels. The 8AMR recorded significantly lower concentrations of SREBP-1c as compared to 8FDR.