“…An investigation of selected biomarkers revealed that the pentose phosphate pathway exhibited the most substantial impact in discriminating different grades of S. ningpoensis Hemsl among the metabolic pathways studied. A more active pentose phosphate pathway results in decreased glucose flux into other metabolic pathways [ 33 ]. As first-grade samples display a more vigorous pentose phosphate pathway compared to second-grade samples, the content of gluconic acid and d -mannose, produced through the oxidation and differential isomerization pathway of glucose, is lower in first-grade samples.…”
“…An investigation of selected biomarkers revealed that the pentose phosphate pathway exhibited the most substantial impact in discriminating different grades of S. ningpoensis Hemsl among the metabolic pathways studied. A more active pentose phosphate pathway results in decreased glucose flux into other metabolic pathways [ 33 ]. As first-grade samples display a more vigorous pentose phosphate pathway compared to second-grade samples, the content of gluconic acid and d -mannose, produced through the oxidation and differential isomerization pathway of glucose, is lower in first-grade samples.…”
“…For example, older sponges and corals regenerate less well (Henry and Hart, 2005), fetal mice can regenerate digit tips at faster rates than adult mice (Borgens, 1982; Han et al, 2003; Tower et al, 2022; Yu et al, 2010), and cardiac regeneration ability decreases with age in mice (Haubner et al, 2012; Santos et al, 2020). In Xenopus laevis tadpoles, limb and tail regeneration is highly dependent on developmental stage (Patel et al, 2022; Poss, 2010; Yun, 2015). These changes in frogs are thought to be related to hormonal state changes after metamorphosis (reviewed in Yun 2015).…”
Regeneration, regrowing lost and injured body parts, is an ability that generally declines with age or developmental transitions (i.e. metamorphosis, sexual maturation) in many organisms. Regeneration is also energetically a costly process, and trade-offs occur between regeneration and other costly processes such as somatic growth, or sexual reproduction. Here we investigate the interplay of regeneration, reproduction, and age in the segmented wormPlatynereis dumerilii.P. dumeriliican regenerate its whole posterior body axis, along with its reproductive cells, thereby having to carry out the two costly processes (somatic and germ cell regeneration) after injury. We specifically examine how age affects the success of germ cell regeneration and sexual maturation in developmentally young versus old organisms. We hypothesized that developmentally younger individuals (i.e. lower investment state, with gametes in early mitotic stages) will have higher regeneration success and reach sexual maturation faster than the individuals at developmentally older stages (i.e. higher investment state, with gametes in the process of maturation). Surprisingly, older amputated worms grew faster and matured earlier than younger amputees, even though they had to regenerate more segments and recuperate the more costly germ cells which were already starting to undergo gametogenesis. To analyze germ cell regeneration across stages, we used Hybridization Chain Reaction for the germline markervasa. We found that regenerated worms start repopulating new segments with germ cell clusters as early as 14 days post amputation. In addition,vasaexpression is observed in a wide region of newly-regenerated segments, which appears different from expression patterns during normal growth or regeneration in worms before gonial cluster expansion. Future studies will focus on determining the exact sources of gonial clusters in regeneration.FundingNIGMS 1R35GM138008-01, Hibbitt Fellowship, WashU Startup funds
“…GLUT4 is the key factor in glucose transport and homeostasis in response to insulin [8] (Figure 1). Upon the uptake of glucose, glucose is phosphorylated to give glucose 6-phosphate/P, which is the forerunner for glycolysis and pentose phosphate pathway (PPP) [9] (Figure 1). Glucose 6-P is metabolized to two pyruvate molecules via the glycolytic pathway [10].…”
Diabetes mellitus is a burdensome disease that affects various cellular functions through altered glucose metabolism. Several reports have linked diabetes to cancer development; however, the exact molecular mechanism of how diabetes-related traits contribute to cancer progression is not fully understood. The current study aimed to explore the molecular mechanism underlying the potential effect of hyperglycemia combined with hyperinsulinemia on the progression of breast cancer cells. To this end, gene dysregulation induced by the exposure of MCF7 breast cancer cells to hyperglycemia (HG), or a combination of hyperglycemia and hyperinsulinemia (HGI), was analyzed using a microarray gene expression assay. Hyperglycemia combined with hyperinsulinemia induced differential expression of 45 genes (greater than or equal to two-fold), which were not shared by other treatments. On the other hand, in silico analysis performed using a publicly available dataset (GEO: GSE150586) revealed differential upregulation of 15 genes in the breast tumor tissues of diabetic patients with breast cancer when compared with breast cancer patients with no diabetes. SLC26A11, ALDH1A3, MED20, PABPC4 and SCP2 were among the top upregulated genes in both microarray data and the in silico analysis. In conclusion, hyperglycemia combined with hyperinsulinemia caused a likely unique signature that contributes to acquiring more carcinogenic traits. Indeed, these findings might potentially add emphasis on how monitoring diabetes-related metabolic alteration as an adjunct to diabetes therapy is important in improving breast cancer outcomes. However, further detailed studies are required to decipher the role of the highlighted genes, in this study, in the pathogenesis of breast cancer in patients with a different glycemic index.
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