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Proteomic and metabolic profile analysis of low-temperature storage responses in Ipomoea batata Lam. tuberous roots

ABSTRACT: Our proteomic and metabolic profile analysis of sweetpotato roots stored at low temperature reveal that the antioxidant enzymes activities, proline and especially soluble sugar content were significantly increased. Most of the DEPs were implicated in phenylpropanoids and followed by starch and sucrose metabolism. Glucosinolate biosynthesis played a leading role in metabolic pathways of sweetpotao roots. More importantly, leucine, tryptophan, tyrosine, isoleucine and valine were all significantly up-regulated in glucosinolate biosynthesis.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Ipomoea Batatas

TISSUE(S): Root

SUBMITTER: Peng Cui

LAB HEAD: Peng Cui

PROVIDER: PXD017728 | Pride | 2021-09-09

REPOSITORIES: Pride

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Proteomic and metabolic profile analysis of low-temperature storage responses in Ipomoea batata Lam. tuberous roots.

Cui Peng P Li Yongxin Y Cui Chenke C Huo Yanrong Y Lu Guoquan G Yang Huqing H

BMC plant biology 20200921 1

<h4>Background</h4>Sweetpotato (Ipomoea batatas L.) is one of the seven major food crops grown worldwide. Cold stress often can cause protein expression pattern and substance contents variations for tuberous roots of sweetpotato during low-temperature storage. Recently, we developed proteometabolic profiles of the fresh sweetpotatoes (cv. Xinxiang) in an attempt to discern the cold stress-responsive mechanism of tuberous root crops during post-harvest storage.<h4>Results</h4>For roots stored und ...[more]

PMID: 32957906

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Project description:Abstract: Non-alcoholic steatohepatitis (NASH) is associated with a disturbed metabolism in liver and excessive accumulation of ectopic fat. Branched-chain amino acids (BCAAs) may beneficially modulate hepatic lipids, however it remains unclear whether individual BCAAs can attenuate already established NASH and oxidative-inflammatory stress associated with it. Therefore, mice were first put on a run-in fast food diet (FFD) for 26 weeks, these obese mice were then treated with individual BCAAs valine or isoleucine (3% of FFD) for another 12 weeks and compared to FFD controls. Valine and isoleucine treatment did not affect obesity, dyslipidemia, gut permeability or fecal fatty acid excretion, although significantly reduced hyperinsulinemia compared with FFD. Valine and isoleucine significantly reduced ALT, CK-18M30, and liver steatosis with a particularly pronounced effect on the microvesicular component (-61% by valine and -71% by isoleucine). Hepatic 4-hydroxynonenal (4-HNE) immunoreactivity, a marker for oxidative stress-induced lipid peroxidation, was also significantly decreased. Functional genomics analysis demonstrated that valine and isoleucine upregulated BCAA metabolism, deactivated master regulators of anabolic pathways related to steatosis (e.g. SREBPF1) and activated master regulators of mitochondrial biogenesis (e.g. PPARGC1a) and lipid catabolism (e.g. ACOX1, AMPK). The correction of critical metabolic pathways by valine and isoleucine was accompanied by a significant decrease of liver inflammation, and suppression of many FFD-stimulated cytokine and chemokine pathways including IL-1β, TNFα and CCR2 signaling. In conclusion, the dietary intervention with either valine or isoleucine corrected multiple metabolic processes in liver and reduced steatosis and inflammation with profound effects on oxidative stress and inflammatory pathways. Methods: Putative antifibrotic effects of butyrate were studied in Ldlr-/-.Leiden mice fed an obesogenic NASH-inducing diet (HFD) containing 2.5% (w/w) butyrate for 38 weeks and compared to an HFD control group. Antifibrotic mechanisms of butyrate were further investigated in TGF-β-stimulated primary human hepatic stellate cells (HSC). Results: HFD-fed mice developed obesity, insulin resistance, increased levels of plasma leptin, adipose tissue inflammation, gut permeability, dysbiosis and NASH-associated fibrosis. Butyrate corrected hyperinsulinemia, lowered plasma leptin levels and attenuated adipose tissue inflammation, without affecting gut permeability or microbiota composition. Butyrate lowered plasma ALT and CK-18M30 and attenuated hepatic steatosis and inflammation. Butyrate inhibited fibrosis development as demonstrated by decreased hepatic collagen content and Sirius-red-positive area. In TGF-β-stimulated HSC, butyrate dose-dependently reduced collagen deposition and decreased procollagen1α1 and PAI-1 protein expression. Transcriptomic analysis and subsequent pathway and upstream regulator analysis revealed deactivation of specific non-canonical TGF-β signaling pathways RhoA/Rock and PI3K/AKT and other important pro-fibrotic regulators (e.g. YAP/TAZ and MYC) by butyrate, providing a potential rationale for its antifibrotic effects. Conclusions: Butyrate protects against the development of obesity and insulin resistance-associated NASH and liver fibrosis. These antifibrotic effects are at least in part attributable to a direct effect on collagen production in hepatic stellate cells, as a result of inhibiting non-canonical TGF-β signaling.

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Proteomic and metabolic profile analysis of low-temperature storage responses in Ipomoea batata Lam. tuberous roots

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Proteomic and metabolic profile analysis of low-temperature storage responses in Ipomoea batata Lam. tuberous roots.

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