Glucose drug resistance

Lyon, R.C., Cohen, I.S., Faustino, PJ Megnin, F., Myers, C.E. (1988). Glucose metabolism in drug-sensitive and drug-resistant human breast cancer cells monitored by magnetic resonance spectroscopy. Cancer Res. 48,870-877. 

The proteins whose abundances are altered in the plasma membrane in drug-resistant cells (Table 13.2) include those involved in increased amino acid uptake (4F2 cell-surface antigen heavy chain, large neutral amino acids transporter small subunit-1), reduced glucose uptake (stomatin, facilitated glucose transport... 

The role of cytoskeletal tubulins in the mode of action and mechanism of drug resistance to benzimidazoles has been reviewed by Lacey [111], who also supports the above hypothesis proposing a close relationship between tubulin-microtubules and other sites of the benzimidazole action. It is believed that inhibition of glucose uptake, fumarate-reductase activity or neuromuscular activity are dependent on inhibition of polymerisation of tubulins to microtubules by benzimidazoles. The inhibition of tubulins by benzimidazoles is so pronounced that it is postulated that even the hatching of eggs of H. controtus is a microtubule dependent process [240]. 

Fu Y, Lee AS. Glucose regulated proteins in cancer progression, drug resistance and immunotherapy. 

Green, C.J. et al. Use of Akt inhibitor and a drug-resistant mutant validates a critical role for protein kinase B/Akt in the msulin-dependent regulation of glucose and system A ammo acid uptake. J. Biol. Chem. 283, 27653-27667 (2008). 

Insulin and Amylin. Insulin is a member of a family of related peptides, the insulin-like growth factors (IGFs), including IGF-I and IGF-II (60) and amylin (75), a 37-amino acid peptide that mimics the secretory pattern of insulin. Amylin is deficient ia type 1 diabetes meUitus but is elevated ia hyperinsulinemic states such as insulin resistance, mild glucose iatolerance, and hypertension (33). Insulin is synthesized ia pancreatic P cells from proinsulin, giving rise to the two peptide chains, 4. and B, of the insulin molecule. IGF-I and IGF-II have stmctures that are homologous to that of proinsulin (see INSULIN AND OTHER ANTIDIABETIC DRUGS). 

The cornerstone of cholera treatment is fluid replacement. Without treatment, the case-fatality rate for severe cholera is approximately 50%. For cholera, rice-based ORT is better than glucose-based ORT because it reduces the number of stools.21 Patients with significant disease should receive a short antibiotic course, 1 to 3 days, to shorten the duration of illness and decrease the number of stools. Doxycycline 300 mg once daily is the drug of choice. Other antibiotics shown to be effective include erythromycin, azithromycin, trimethoprim-sulfamethoxazole, and ciprofloxacin.2 Antibiotic resistance has been documented in V cholerae since 1977.2 Antibiotic prophylaxis is not warranted. 

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