Dietary fat and protein intake differ in modulation of prostate tumor growth, prolactin secretion and metabolism, and prostate gland prolactin binding capacity in rats.
The combined effects of dietary fat and protein concentration on prostate tumor growth and endocrine homeostasis were evaluated in male rats. A 2 x 2 factorial experiment examined the effects of protein (5 and 20% of energy as casein) and fat (10 and 40% of energy as corn oil) on the growth of the Dunning R3327-H transplantable prostate adenocarcinoma in Copenhagen x Fisher F1 rats. Rats fed protein-restricted diets for 20 wk exhibited lower energy intakes, final body weights and tumor growth rates. Weanling male Sprague-Dawley rats fed protein-restricted diets for 4 wk had serum concentrations of prolactin, growth hormone and testosterone which were 68, 17 and 85% of controls, respectively. After 16 wk of feeding, there were no effects of dietary protein on serum hormone concentrations despite reduced energy intake and body weight. The metabolic clearance rate of serum prolactin was lower in rats fed the low protein diets for 4 or 16 wk; however, no differences were noted when adjusted for body weight. In vivo studies employing intravenously injected 125I-labeled prolactin revealed slight alterations in the metabolism of circulating prolactin monomer or binding to serum proteins in protein-restricted rats. The maximal binding capacity of prolactin receptors on the prostate membrane fraction was 42% lower in rats fed diets restricted in protein despite normal serum hormone concentrations at 16 wk. Dietary fat had no effect on tumor growth or prolactin homeostasis although a slightly greater serum testosterone was noted in rats fed high fat diets. In contrast, restriction of dietary protein caused significant changes in energy intake, serum hormone concentrations, prolactin metabolism, prostatic prolactin binding capacity and prostate tumor growth rates. These studies support the hypothesis that dietary protein and energy intake, particularly during periods of rapid growth and development, may alter prostate biology and modulate the risk of future prostate cancer progression.
Clinton
S K
SK
Division of Cancer Pharmacology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.
Mulloy
A L
AL
Li
S P
SP
Mangian
H J
HJ
Visek
W J
WJ
D000230:Adenocarcinoma / Q000178:diet therapy / Q000473:pathology*; D000818:Animals; D001835:Body Weight; D004041:Dietary Fats / Q000008:administration & dosage* / Q000627:therapeutic use; D004044:Dietary Proteins / Q000008:administration & dosage* / Q000627:therapeutic use; D002149:Energy Intake; D013006:Growth Hormone / Q000097:blood; D008297:Male; D008657:Metabolic Clearance Rate; D009929:Organ Size; D010902:Pituitary Gland / Q000033:anatomy & histology / Q000378:metabolism; D011388:Prolactin / Q000097:blood / Q000378:metabolism*; D011467:Prostate / Q000378:metabolism*; D011471:Prostatic Neoplasms / Q000178:diet therapy / Q000473:pathology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D011981:Receptors, Prolactin / Q000378:metabolism; D013739:Testosterone / Q000097:blood
D004041:Dietary Fats; D004044:Dietary Proteins; D011981:Receptors, Prolactin; D013739:Testosterone; D011388:Prolactin; D013006:Growth Hormone