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Metabolic Syndrome
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Increased leptin levels, seen in obesity and metabolic syndrome, are linked to breast, colon, endometrial, and prostate cancers. Leptin increases production of metalloproteinases and promotes angiogenesis. Therefore, it is related to increased metastatic activities. Vascular endothelial growth factor (VEGF) is produced in greater quantities because of the effects of estrogen, hypoxia, insulin-like growth factor 1, insulin, tumor necrosis factor-alpha, and leptin. Metabolic syndrome increases VEGF levels, increasing angiogenesis, tumor progression, and metastases. Because of high metabolism, cancer cells have increased needs for glucose. The cells speed up the activity of glucose transporters. Therefore, energy restriction inhibits tumor development and progression. In diabetic or glucose-intolerant patients, increased supply of glucose may explain increased risks for some types of cancer and related deaths.
Hyperkinetic Movement Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Morales-Briceno Hugo, Victor S.C. Fung, Annu Aggarwal, Philip Thompson
Metabolic: Thiamine responsive basal ganglia disease.Mitochondrial thiamine transporter deficiency.Lesch–Nyhan syndrome (LNS).Glucose transporter type 1 deficiency (GLUT1).
Glycogenosis type I – von Gierke disease
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
The glucose-6-phosphatase system also depends on the transport of glucose. A number of glucose transport proteins has been identified and they have been designated GLUT 1–6. Deficiency of GLUT 2 causes the syndrome of hepatic glycogenosis in the Fanconi-Bickel syndrome [81].
In vitro Anti-colorectal Cancer Potential of the Medicinal Mushroom Ganoderma neo-japonicum Imazeki in Hyperglycemic Condition: Impact on Oxidative Stress, Cell Cycle and Apoptosis
Published in Nutrition and Cancer, 2022
Meng-Fei Lau, Kek-Heng Chua, Vikineswary Sabaratnam, Umah Rani Kuppusamy
Adenosine triphosphate (ATP) is the universal carrier of energy in all living cells. It is exclusively synthesized through mitochondrial oxidative phosphorylation. Cancer cells, however, commit cytoplasmic glycolysis in sustaining their energy demand even at normoxic condition (57). This metabolic shift (known as “Warburg effect”) is often accompanied by enhanced glucose ingestion. Cellular glucose uptake is facilitated by glucose transporters (GluT). Under HG culture (control), the surplus of glucose availability promoted glucose uptake in HCT 116 cells (Figure 5A) as opposed to HT 29 cells (Figure 5B). It was a cell type-dependent response, conforming to the phenomenon reported on thyroid cancer carcinomas with different GluT expression profiles (58). High glucose induces oxidative stress via glucose autoxidation (59). Hence, in parallel to glycolysis, the PPP flux is initiated so that the metabolic needs for NADPH can be complemented under hyperglycemic conditions (44). Since several rate-limiting enzymes regulate the interplay between glycolysis and PPP, the cellular GSH levels remained constant (Figure 3) despite the increased glucose uptake upon treatment with Hex fraction (Figure 5). In contrast, Chl fraction gave rise to GSH depletion (Figure 3) with or without the reduction of glucose uptake (Figure 5) suggesting its interruptions in the enzymatic activity of GSH regeneration which involves glucose-6-phosphate dehydrogenase, glutathione reductase, and glutathione peroxidase.
Understanding glomerular diseases through proteomics
Published in Expert Review of Proteomics, 2021
E. Mavrogeorgis, H. Mischak, J. Beige, A. Latosinska, J. Siwy
The treatment of CKD is also still moderately effective. One reason appears the diverse disease etiology. A large proportion of CKDs (e.g., diabetic kidney disease (DKD), hypertensive nephropathy (HN), IgA nephropathy (IgAN)) is associated with increased blood pressure (BP) [11], which also is thought to be responsible at least in part for the glomerular damage observed. As a consequence, BP lowering was and is one of the main principles in treatment [11]. The benefits of interfering with the renin angiotensin aldosterone system (RAAS) have been demonstrated in multiple studies. In these studies, it also became evident that earlier intervention delivers the highest absolute benefit [8]. Recently, a second type of drugs, sodium-dependent glucose transporter-2 (SGLT-2) inhibitors that interfere with the tubular glucose reabsorption, have been successfully introduced [12]. These drugs consistently delivered additional reno-protective benefit, on top of RAAS inhibition [13]. However, even though obviously substantial progress has been made, CKD is still an incurable disease that includes a number of potential complications, such as cardiovascular disease (CVD) and ESKD, requiring Kidney Failure Replacement Therapy. Moreover, CKD is associated with substantially reduced life expectancy (up to 16 years, depending on the age at onset and the disease stage) [14].
Higher Glucose Enhances Breast Cancer Cell Aggressiveness
Published in Nutrition and Cancer, 2020
Julianna M. Santos, Fazle Hussain
Our finding that an increase in expression of key glycolytic enzymes requires an increase in glucose uptake, prompted us to study the effect of higher glucose on glucose uptake. MCF-7 (Fig. 3a–f) and MB231 (Fig. 3h–m) fluorescent micrographs, accompanied by their inverted images, after incubation with a glucose analog conjugated to a fluorescent molecule (2-NBDG, fluorescently-tagged glucose derivative). Cells were kept in culture media for 72 h with different D-(+)-glucose concentrations: 5 (physiological) and higher 15 and 30 mM. The fluorescence intensity was quantified for MCF-7 (Fig. 3g) and MB231 (Fig. 3n). The former did not show a significant increase in glucose uptake, whereas the latter increased significantly the glucose uptake with 30 mM glucose. These results corroborate our previous finding that MB231 is more glucose dependent than MCF-7. In addition, higher glucose can induce overexpression of glucose transporters reflecting an increased glucose uptake. Thus, the glucose dependence is not just related to increase of expression of glycolytic enzymes but also the increase in glucose uptake.