The objective of the study was to assess the effect of dietary incorporation of different feed attractants viz. tubifex, earthworm and fish meal on growth and survival of O. bimaculatus (pabda fish) fry. Fifty numbers of fifteen days weaned fry (0.105±0.008g; 2.14±0.14cm) were stocked into each aerated aquariums (30.0 x 15.0 x 15.0 cm) following a completely randomized design (CRD) consisting of four treatments including the control with three replicates each. Four iso-nitrogenous purified diets were prepared including three treatment diets with attractants (5%) by replacing an appropriate amount of casein and cellulose and fed to the fishes twice daily. Results from the study showed that growth of fry as measured by final weight, weight gain, mean daily weight gain and specific growth rate of fries were significantly (p<0.05) higher in tubifex supplemented group and lower in control group. Survival was significantly higher in tubifex supplemented group (42.66±1.3%) and lower in control group. Moreover, other yield parameters such as total biomass, condition factor and performance index also followed the same trend as survival. Further, higher protease activity was-1-1 found in control group (2.233±0.038 units mg protein min) followed by earthworm (0.354±0.031 mg-1-1 protein min) supplemented group (p<0.05). The lipase and amylase activity were higher (p<0.05) in tubifex and control groups, respectively. It could be concluded that the dietary supplementation of tubifex at 5% inclusion level could be a promising aquaculture feeding strategy for pabda fish due to its rich nutrient content, increased feeding stimulation and more palatability.
Nonalcoholic fatty liver disease (NAFLD) is an independent predictor of systemic insulin resistance and type 2 diabetes mellitus (T2DM). However, converse correlates between excess liver fat content and β-cell function remain equivocal. Specifically, how the accumulation of liver fat consequent to the enhanced de novo lipogenesis (DNL) leads to pancreatic β-cell failure and eventually to T2DM is elusive. Here we have identified lowmolecular-weight calcium-binding protein S100A6 or calcyclin inhibits glucose-stimulated insulin secretion (GSIS) from β-cells through activation of the receptor for the advanced glycation end product (RAGE) and diminution of mitochondrial respiration. Serum S100A6 level is elevated both in human NAFLD patients and in a high-fat diet (HFD) induced mouse model of NAFLD. While serum S100A6 levels are negatively associated with β-cell insulin secretory capacity in human patients, depletion of hepatic S100A6 improves GSIS and glycemia in mice suggesting that S100A6 contributes to the pathophysiology of diabetes in NAFLD. Moreover, transcriptional induction of hepatic S100A6 is driven by the potent regulator of DNL, carbohydrate response element-binding protein (ChREBP), and ectopic expression of ChREBP in the liver suppresses GSIS in a S100A6 sensitive manner. Together, these data suggest elevated serum levels of S100A6 may serve as a biomarker in identifying NAFLD patients with a heightened risk of developing β-cell dysfunction. Overall, our data, implicate S100A6 as a hitherto unknown hepatokine to be activated by ChREBP and participates in the hepato-pancreatic communication to impair insulin secretion and drive the development of T2DM in NAFLD.
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