38 research outputs found

    Pengaruh Lama Waktu Fermentasi terhadap Kadar Bioetanol dari Pati Ubi Jalar Kuning (Ipomea Batata L)

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    The sweet potato is yellow is one that the carbohydrate that is high, so it can be used as one of the alternative raw materials for bioethanol. This study aims to determine the levels of ethanol sweet potato is yellow through fermentation with the use of yeast bread with a variety of time 3, 4, 5, 6, dan 7 days at room temperature. The results of the research showed glucose levels derived from the process of hydrolysis using acid HCl 21% were of 4.54% with high levels ethanol that optimum obtained through fermentation use of yeast Saccharomyces cerevisiae of 9.70% over fermentation 5 days

    PI3K-C2 alpha Knockdown Results in Rerouting of Insulin Signaling and Pancreatic Beta Cell Proliferation

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    Insulin resistance is a syndrome that affects multiple insulin target tissues, each having different biological functions regulated by insulin. A remaining question is to mechanistically explain how an insulin target cell/tissue can be insulin resistant in one biological function and insulin sensitive in another at the same time. Here, we provide evidence that in pancreatic beta cells, knockdown of PI3K-C2 alpha expression results in rerouting of the insulin signal from insulin receptor (IR)-B/PI3K-C2 alpha/PKB-mediated metabolic signaling to IR-B/Shc/ERK-mediated mitogenic signaling, which allows the beta cell to switch from a highly glucose-responsive, differentiated state to a proliferative state. Our data suggest the existence of IR-cascade-selective insulin resistance, which allows rerouting of the insulin signal within the same target cell. Hence, factors involved in the rerouting of the insulin signal represent tentative therapeutic targets in the treatment of insulin resistance.11108Ysciescopu

    Pengaruh Lama Waktu Fermentasi Terhadap Kadar Bioetanol dari Pati Ubi Jalar Kuning (Ipomea batata L)

    Get PDF
    The sweet potato is yellow is one that the carbohydrate that is high, so it can be used as one of the alternative raw materials for bioethanol. This study aims to determine the levels of ethanol sweet potato is yellow through fermentation with the use of yeast bread with a variety of time 3, 4, 5, 6, dan 7 days at room temperature. The results of the research showed glucose levels derived from the process of hydrolysis using acid HCl 21% were of 4.54% with high levels ethanol that optimum obtained through fermentation use of yeast Saccharomyces cerevisiae of 9.70% over fermentation 5 days

    Expression of truncated Kir6.2 promotes insertion of functionally inverted ATP-sensitive K+ channels

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    ATP-sensitive K+ (KATP) channels couple cellular metabolism to electrical activity in many cell types. Wild-type KATP channels are comprised of four pore forming (Kir6.x) and four regulatory (sulfonylurea receptor, SURx) subunits that each contain RKR endoplasmic reticulum retention sequences that serve to properly translocate the channel to the plasma membrane. Truncated Kir6.x variants lacking RKR sequences facilitate plasma membrane expression of functional Kir6.x in the absence of SURx; however, the effects of channel truncation on plasma membrane orientation have not been explored. To investigate the role of truncation on plasma membrane orientation of ATP sensitive K+ channels, three truncated variants of Kir6.2 were used (Kir6.2ΔC26, 6xHis-Kir6.2ΔC26, and 6xHis-EGFP-Kir6.2ΔC26). Oocyte expression of Kir6.2ΔC26 shows the presence of a population of inverted inserted channels in the plasma membrane, which is not present when co-expressed with SUR1. Immunocytochemical staining of intact and permeabilized HEK293 cells revealed that the N-terminus of 6xHis-Kir6.2ΔC26 was accessible on both sides of the plasma membrane at roughly equivalent ratios, whereas the N-terminus of 6xHis-EGFP-Kir6.2Δ26 was only accessible on the intracellular face. In HEK293 cells, whole-cell electrophysiological recordings showed a ca. 50% reduction in K+ current upon addition of ATP to the extracellular solution for 6xHis-Kir6.2ΔC26, though sensitivity to extracellular ATP was not observed in 6xHis-EGFP-Kir6.2ΔC26. Importantly, the population of channels that is inverted exhibited similar function to properly inserted channels within the plasma membrane. Taken together, these data suggest that in the absence of SURx, inverted channels can be formed from truncated Kir6.x subunits that are functionally active which may provide a new model for testing pharmacological modulators of Kir6.x, but also indicates the need for added caution when using truncated Kir6.2 mutants. © 2021, The Author(s).Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

    Glucagon regulates its own synthesis by autocrine signaling

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    Peptide hormones are powerful regulators of various biological processes. To guarantee continuous availability and function, peptide hormone secretion must be tightly coupled to its biosynthesis. A simple but efficient way to provide such regulation is through an autocrine feedback mechanism in which the secreted hormone is “sensed” by its respective receptor and initiates synthesis at the level of transcription and/or translation. Such a secretion–biosynthesis coupling has been demonstrated for insulin; however, because of insulin’s unique role as the sole blood glucose-decreasing peptide hormone, this coupling is considered an exception rather than a more generally used mechanism. Here we provide evidence of a secretion–biosynthesis coupling for glucagon, one of several peptide hormones that increase blood glucose levels. We show that glucagon, secreted by the pancreatic α cell, up-regulates the expression of its own gene by signaling through the glucagon receptor, PKC, and PKA, supporting the more general applicability of an autocrine feedback mechanism in regulation of peptide hormone synthesis

    Ciliary dysfunction impairs beta-cell insulin secretion and promotes development of type 2 diabetes in rodents.

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    Type 2 diabetes mellitus is affecting more than 382 million people worldwide. Although much progress has been made, a comprehensive understanding of the underlying disease mechanism is still lacking. Here we report a role for the β-cell primary cilium in type 2 diabetes susceptibility. We find impaired ​glucose handling in young ​Bbs4−/− mice before the onset of obesity. Basal body/ciliary perturbation in murine pancreatic islets leads to impaired first phase insulin release ex and in vivo. ​Insulin receptor is recruited to the cilium of stimulated β-cells and ciliary/basal body integrity is required for activation of downstream targets of insulin signalling. We also observe a reduction in the number of ciliated β-cells along with misregulated ciliary/basal body gene expression in pancreatic islets in a diabetic rat model. We suggest that ciliary function is implicated in insulin secretion and insulin signalling in the β-cell and that ciliary dysfunction could contribute to type 2 diabetes susceptibility
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