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The Effects of Fenugreek on Controlling Glucose in Diabetes Mellitus
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Zahra Ayati, Nazli Namazi, Mohammad Hossein Ayati, Seyed Ahmad Emami, Dennis Chang
It is well established that abnormal gut microbiota composition is linked with metabolic disorders, including obesity and diabetes. Galactomannan, the water-soluble polysaccharides in fenugreek gum, has been considered to have the potential to regulate gut microbiota and improve glucose metabolism. In an in vivo study on mice, administration of galactomannan in the diet altered microbiota population in the gut. It also increased adenosine monophosphate-activated protein kinase (AMPK) activation in the liver. AMPK is considered as a regulator of glucose metabolism in the liver, which inhibits the activity of acetyl-coenzyme A carboxylase (ACC) and thus leads to a decrease of lipogenesis (56). A metabonomic study evaluated the underlying antidiabetic mechanism of fenugreek galactomannan in streptozotocin-induced diabetic rats. The results of urine and serum analysis of treated rats revealed that administration of galactomannan modifies a range of biomarkers which are involved in energy metabolism and several other metabolisms, such as phenylalanine, histidine, tryptophan, sphingolipid, glycerophospholipid and arachidonic acid (57). Galactomannan is also suggested to improve and protect the pancreas function. In an in vivo study on diabetic mice, administration of galactomannan protected the pancreas from histological changes (58).
Signalling Pathways in The Regulation of Cellular Responses to Exercise
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Anders Gudiksen, Stine Ringholm, Henriette Pilegaard
Conserving cellular ATP levels during muscle contractions is vital to maintain cell function. Adenosine monophosphate (AMP)-activated protein kinase (AMPK) is highly responsive to metabolic perturbations and is acutely activated to re-establish cellular energy homeostasis through phosphorylation of key metabolic enzymes. AMPK activation turns on catalytic ATP-generating processes while inhibiting anabolic processes such as lipid and protein synthesis. The highly conserved AMPK is a heterotrimeric kinase consisting of a catalytic α as well as a regulatory β and γ subunit, all of which are found in multiple isoform complexes (45, 111). AMP-binding sites and a glycogen-binding domain are contained within the β subunit, which presumably acts to inhibit the activity of the kinase when glycogen stores are abundant (97). AMPK is allosterically inhibited by creatine phosphate and activated several-fold by an increase in cytosolic AMP/ATP ratio (11, 31). Binding of AMP to AMPK allows exposure of the threonine residue on the α subunit, which is phosphorylated by the upstream AMPK kinases constitutively active tumour suppressor liver kinase B1 (LKB1)(133) and CAMK kinase β (48, 132) (Figure 8.2).
Mupirocin
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Isoleucyl–tRNA synthesis occurs in two steps. First, the intermediate isoleucyl-adenylate (isoleucyl–adenosine monophosphate [AMP]) is generated from isoleucine and adenosine triphosphate (ATP). The second step involves the transfer of this intermediate to the 3′-terminus of the corresponding tRNA. This isoleucyl–tRNA complex subsequently delivers the isoleucines to ribosomes during protein synthesis. Mupirocin acts as an analog of isoleucyl-AMP by binding to the catalytic cleft of the tRNA synthetase, called the Rossman fold domain. Competitive inhibition of this enzyme arrests protein synthesis (Hughes and Mellows, 1978).
Gypenosides counteract hepatic steatosis and intestinal barrier injury in rats with metabolic associated fatty liver disease by modulating the adenosine monophosphate activated protein kinase and Toll-like receptor 4/nuclear factor kappa B pathways
Published in Pharmaceutical Biology, 2022
Shuhua Shen, Kungen Wang, Yihui Zhi, Yue Dong
Gypenosides (GP) are the main phytochemical component of Gynostemma pentaphylla (Thunb.) Makino (Cucurbitaceae) which is reported to have diverse pharmacological effects including antioxidation, immunomodulation, antitumor, antifatigue, neuroprotection and hepatoprotection (Wang et al. 2017; Ji et al. 2018). Gynostemma pentaphylla is an herbaceous climbing vine widely grown in South and East Asia (Lee et al. 2019). The aforementioned effects of Gynostemma pentaphylla have been reported to be associated with the molecular weight, monosaccharide composition and chemical structure of the extracted GP (Ji et al. 2018). Moreover, Lee et al. (2019) demonstrated that GP can strengthen adenosine monophosphate activated protein kinase (AMPK) activation to reduce the high fat-induced obesity in mice (Neuschwander-Tetri 2017). In addition, it has been reported that AMPK and NF-κB signalling pathways play a regulatory role in the pathological process of liver injury, hepatic steatosis and hepatic fibrosis (Yang et al. 2020; Li et al. 2021). However, whether GP can regulate AMPK activation to affect the progression of MAFLD is undetermined yet.
PLD1 knockdown reduces metastasis and inflammation of fibroblast-like synoviocytes in rheumatoid arthritis by modulating NF-κB and Wnt/β-catenin pathways
Published in Autoimmunity, 2021
Zhengyu Zhang, Xi Chen, Bo Gao, Guomin Sun, Yan Wang, Junke Wang, Ting Zhang, Hao Qian, Yu Zhang, Jun Huang, Rurong Sun, Jiabiao Wu, Lei Zhou
Similar to malignant cells, the proliferation of RA-FLSs leads to the increase of intracellular inflammatory factors [4,18]. Inflammatory transmitters, such as IL-1, IL-6 and tumour necrosis factor-α (TNF-α), could be detected in the synovium of RA patients [19]. PLD can be activated by a variety of inflammatory mediators to dehydrolyze PC, which is related to cell proliferation, cell division, calcium mobilisation, as well as specific protein kinase activation [4]. It has been reported that the mechanism of some anti-inflammatory drugs may be partly associated with the inhibition of PLD. In addition, drugs that increase cellular cyclic adenosine monophosphate levels were reported to inhibit cellular PLD activity . These studies are also consistent with our speculation that elevated PLD1 expression in RA might be associated with the inflammatory symptoms experienced by RA patients. In this study, we confirmed that inhibition of PLD1 expression reduced the levels of inflammatory factors by ELISA, such as L-1β, TNF-α, IL-6, IFN-γ, and MCP-1 in RA-FLSs, which in turn reduced the degree of inflammation.
Targeting circadian PER2 as therapy in myocardial ischemia and reperfusion injury
Published in Chronobiology International, 2021
Yoshimasa Oyama, Lori A Walker, Tobias Eckle
Interestingly, the discovery of light elicited PER2 was initially based on studies investigating adenosine signaling in cardioprotection. Extracellular adenosine signaling is an essential cellular adaptive mechanism (Fredholm 2007; Ohta and Sitkovsky 2001; Sitkovsky et al. 2004; Thiel et al. 2005). In the extracellular space, adenosine originates from 5ʹ-adenosine monophosphate (AMP) via ecto-5ʹ-nucleotidase (CD73) mediated phosphohydrolysis. Adenosine then signals through four well-described adenosine receptors, the ADORA1, ADORA2A, ADORA2B, or ADORA3 (Fredholm 2007; Hasko et al. 2008). During hypoxia or ischemia, extracellular adenosine production and signaling increase significantly (Eckle et al. 2008b, 2007). Enhanced activation of adenosine receptors can then mediate endothelial barrier protective or anti-inflammatory effects (Eckle et al. 2008a; Eltzschig et al. 2004; Rosenberger et al. 2009). These adenosine signaling effects are ultimately organ protective during ischemia (Hart et al. 2008; Lappas et al. 2006; Linden 2006; Yang et al. 2005). On the other side, genetic ablation of ADORA2B signaling abolishes ischemic-preconditioning elicited cardioprotection (Eckle et al. 2008c; Eltzschig 2009; Kohler et al. 2007). Interestingly, ischemic preconditioning, where short non-lethal ischemic periods precede a more extended ischemic period, has been described as the most potent cardioprotective mechanism discovered at the bench. Regardless, these studies implicate adenosine signaling events as a central mechanism in cardioprotection.