Insulin binding and glucose transport in the R3230AC mammary adenocarcinoma

✍ Scribed by Harmon, Joan Thilly ;Hilf, Russell

• Book ID: 102438426
• Publisher: Wiley (John Wiley & Sons)
• Year: 1976
• Tongue: English
• Weight: 351 KB
• Volume: 4
• Category: Article
• ISSN: 0091-7419
• DOI: 10.1002/jss.400040210

✦ Synopsis

Abstract

Cells dissociated from the R3230AC mammary adenocarcinoma from intact and diabetic rats were examined for insulin binding and glucose transport. The K~d~ for insulin binding, ∼ 10^−10^ M, was similar in all tumors studied. However, the apparent number of receptor sites per cell increased in cells from diabetic rats. Kinetic analysis of 3‐0‐methyl glucose (3‐OMG) entry showed both diffusional and passive carrier characteristics. Insulin (4 × 10^−9^ M) in vitro did not affect diffusional entry, whereas the hormone altered the passive carrier system, as reflected by an increase in K~m~ and V~max~. Insulin decreased initial velocity of glucose transport at 4–6 mM glucose levels but increased initial velocity of glucose transport at 20 mM glucose. An explanation of the role of insulin on tumor growth in vivo from effects on glucose transport in vitro is proposed.