in dietary cellulose significantly reduces the incidence of colonic adenocarcinomas in a dose-dependent manner without detrimental side effects, (e) Cellulose is already approved as a human food supplement. DAVID W. HEITMAN* IVAN L. CAMERON
Department of Cellular and Structural Biology The University of Texas Health Science Center San Antonio, Tex
( / / ) FREEMAN HJ, SPILLER GA, KIM YS: A dou-
ble-blind study on the effects of differing purified cellulose and pectin fiber diets on 1,2-dimethylhydrazine-induced rat colonic neoplasia. Cancer Res 40:2661-2665, 1980 (12) HHTMAN DW, ORD VA, HUNTER KE, ET AL:
Effect of dietary cellulose on cell proliferation and progression of 1,2-dimethylhydrazineinduced colon carcinogenesis in rats. Cancel Res 49:5581-5585, 1989 (13) LJPKIN M: Biomarkers of increased susceptibility of gastrointestinal cancer. Their development and application to studies of cancer prevention. Gastroenterology 92:1083-1086, 1987 (14) LJPKIN M: Biomarkers of increased susceptibility to gastrointestinal cancer. New application to studies of cancer prevention in human subjects. Cancer Res 48:235-245, 1988 (15) COLE JW, MCKALEN A: Studies on the mor-
References
phogenesis of adenomatous polyps in the human colon. Cancer 16:998-1002, 1963 (16) DESCHNER EE, LEWIS CM, LJPKIN M: In vitro
(/) DECOSSE JJ, MILLER HH, LESSER ML: Effect
(6) NATIONAL ACADEMY OF SCIENCE, NATIONAL
RESEARCH COUNCIL: Diet, Nutrition, and
Cancer. Washington, DC: National Academy Press, 1982 (7) JACOBS LR, LUPTON JR: Relationship be-
tween colonic Iuminal pH, cell proliferation, and colon carcinogenesis in 1,2-dimethylhydrazine-treated rats fed high fiber diets. Cancer Res 46:1727-1734, 1986 (8) FREEMAN HJ, SPILLER GA, KIM YS: A dou-
ble-blind study on the effect of purified cellulose dietary fiber on 1,2-dimethylhydrazineinduced rat colonic neoplasia. Cancer Res 38:2912-2917, 1978 (9) BAUER HG, ASP NG, OSTER.ETAL: Effect of
dietary fiber on the induction of colorectal tumors and fecal fj-glucuronidase activity in the rat. Cancer Res 39:3752-3756, 1979 (70) NIGRO ND, BULL SW, KLOPFER BA, ET AL:
Effect of dietary fiber on azoxymethane-induced intestinal carcinogenesis in rats. JNCI 62:1097-1102,1979
Vol. 82, No. 13, July 4, 1990
Reference (/) DECOSSE JJ, MILLER HH, LESSER ML: Effect
of wheat fiber and vitamins C and E on rectal polyps in patients with familial adenomatous polyposis. J Natl Cancer Inst 81:1290-1297, 1989
study of human epithelial cells. I. Atypical zone of H3-thymidine incorporation in mucosa of multiple polyposis. J Clin Invest 42:1922-1928, 1963 (17) DESCHNER EE, LJPKIN M, SOLOMON C: Study
of human rectal epithelial cells in vitro. U. H3-thymidine incorporation into polyps and adjacent mucosa. J Natl Cancer Inst 36:849-857, 1966
Response
(5) ROGERS AE, NAUS KM: Contributions of
laboratory animal studies of colon carcinogenesis. In Large Bowel Cancer (Mastromarino AJ, Brattain MG, eds). New York: Praeger, 1984, pp 1-45
JEROME J. DECOSSE
Department of Surgery (F-1917) The New York HospitalCornell Medical Center 525 E. 68th St. New York, NY 10021
Drs. Heitman and Cameron address our recent article (7) in which we reported that a wheat bran supplement in excess of 11 g/day was associated with regression of rectal polyps in patients with familial adenomatous polyposis. The gist of their letter is that cellulose is the effective component of insoluble fiber and that human trials should now be initiated with cellulose. The data provided on cellulose are interesting and, indeed, trials of insoluble fiber need to be initiated in patients with an average risk of colon cancer. However, as a fundamental strategy in extending a study, one should go with what seems to work, namely, wheat bran, not one of its components. Moreover, in a long-term study that may extend beyond 5 years, the palatability of the treatment agent is critically important. Developing a reliably palatable form of cellulose would be a prerequisite for a cellulose trial. Finally, studies in
Gastrointestinal Peptide Hormones and Breast Cancer The recent paper by Goettler et al. (7) raises the issue of whether changes in gastrointestinal (GI) response are predisposing factors in the development of breast cancer. As noted by Goettler et al., we have reported a higher release of gastrin, but no release of vasoactive intestinal polypeptide or neurotensin in premenopausal patients with breast cancer (2-4). However, a number of conditions are related to such data. Initially, we compared the GI peptide hormone response to isocaloric carbohydrate or "fat" breakfasts in three groups of healthy premenopausal women, body mass index less than 23, 24-27, or more than 28, and in women with stage LT breast cancer to age- and weight-
Downloaded from http://jnci.oxfordjournals.org/ at Harvard University on July 11, 2015
of wheat fiber and vitamins C and E on rectal polyps in patients with familial adenomatous polyposis. J Natl Cancer Inst 81:1290-1297, 1989 (2) JACOBS LR: Enhancement of rat colon carcinogenesis by wheat bran consumption during the stage of 1,2-dimethylhydrazine administration. Cancer Res 43:4057-4061, 1983 (3) ZARIDZE DG: Environmental etiology of large-bowel cancer. JNCI 70:389^00, 1983 (4) WnxETT WC, MACMAHON B: Diet and cancer—an overview. I and D. N Engl J Med 310:633-^38,697-703,1984
patients with an average risk of colon cancer must also recognize the potential importance of a low-fat diet in risk reduction.
*Correspondence to: Peter Hill, Ph.D., Mahoney Institute, American Health Foundation, 320 E. 43rd St., New York, NY 10017.
CORRESPONDENCE 1155
As reported by Goettler et al. (7) in postmenopausal patients, we reported a higher gastrin release in premenopausal patients after a fat meal than in the ageand weight-matched control subjects. The increase in plasma vasoactive intestinal polypeptide in the control group after a fat meal was not found in patients with breast cancer (3). No increase in vasoactive intestinal polypeptide occurred after a carbohydrate meal in the control group. While these findings are ostensibly similar to those of Goettler et al. (7), the difference in response due to the effects of body mass index or administration of naloxone or cholecystokinin evident between lean women with a body mass index that was less than 23 and obese women with a body mass index greater than 28, implies a difference in their physiological status. Overlapping responses occurred in women whose body mass index was 24-27 (7). This finding applied to our observations in age- and weight-matched controls with a body mass index of 24.7 ± 0.73 and could apply to the results obtained by Goettler etal. (7). This problem applies to neurotensin release in response to naloxone and cholecystokinin, where cholecystokinin suppresses neurotensin release only in obese women, body mass index greater than 28, while naloxone suppresses neurotensin release in lean women, but in-
1156
creases neurotensin release in obese women (2,6). Since behavioral stress affects digestion (9,70), differences in GI response can be modified in patients, leading to anomalies such as an unexpected weight gain in some premenopausal patients receiving chemotherapy. It is of interest that gastrin and vasoactive intestinal polypeptide responses to a fat meal are similar in premenopausal and postmenopausal patients since gonadal steroids not only affect a number of central nervous system peptide hormones, opioids, neuropeptide Y, and substance P (peptide hormones associated with digestion and release of luteinizing hormone-releasing hormone-luteinizing hormone release), but also food intake (77), GI transit time (72), and GI peptide hormone release (13). Although a high frequency of concomitant gynecologic and digestive dysfunction (14,15) does not prove causality, a common gonadal honnone dysfunction is suggested in these patients. We concur with Goettler et al. (7) that changes in prolactin metabolism are predominantly related to protein (16,17). Accordingly, the findings of Goettler et al. and our data indicate a previously neglected step between luminal nutrients and circulating nutrients that may play a major role in controlling differentiation of growth factors in diet-hormone-related diseases. PETER HILL*
Mahoney Institute American Health Foundation New York, NY
References (1) GOETTLER DM, LEVINE L, CHEY WY: Post-
prandial levels of prolactin and gut hormones in breast cancer patients: Association with stage of disease, but not dietary fat. J Nat! Cancer Inst 82:22-28, 1990 (2) KOPPESCHAAR HPP, HILL P, GARBACZEWSKI
L, ET AL: Effect of meals, naloxone and cholecystokinin on plasma neurotensin levels in lean and obese women. Presented at the 4th International Congress on Obesity, Stockholm, Sweden, June 1989 (3) Hm. P, DE WAARD F, THUSSEN JHH, ET AL:
Gut-CNS peptide hormones in healthy women and breast cancer patients. Presented at the 3rd Annual European Cancer Prevention Symposium, Aarhus, Denmark, 1985 (4) HEX P, GARBACZEWSKI L, THUSSEN
(6) HILL P, GARBACZEWSKI L, KOOPESCHAAR
HPP, ET AL: Peptide hormones, digestion and menstrual periodicity. In The Menstrual Cycle and Its Disorders (Pirke KM, Luuttke K, Schweiger V, eds). Berlin: Springer-Verlag, 1989, pp 133-141 (7) HILL P,
Jos H. H. THUSSEN
HANS KOPPERSCHAAR
Department of Endocrinology Utrecht University Hospital Utrecht, The Netherlands
GARBACZEWSKI L, KOPPESCHAAR
HPP, ET AL: Glucagon and insulin response to meals in non-obese and obese Dutch women. ClinChim Acta 165:253-263, 1987 (8) HILL P,
GARBACZEWSKI L, KOPPESCHAAR
HPP, ET AL: Peptides and steroid hormones in subjects at different risk for diet-related diseases. Am J Clin Nutr 48:782-786, 1988 (9) WELOAN P, MESHKINPOUR H, BEELER M:
Effect of anger on colon motor and myoelectric activity in irritable bowel syndrome. Gastroenterology 94:1150-1156, 1988 (10) HOLTMANNG,SINGERMV.KREIBELR,ETAL:
Differential effects of acute mental stress on interdigestive secretion of gastric acid, pancreatic enzymes and gastroduodenal motility. Dig Dis Sci 34:1701-1707, 1989 (11) DALVTT SP: The effect of the menstrual cycle on patterns of food intake. Am J Clin Nutr 34:1811-1815,1981 (12) WALD A, VAN THIEL DH, HOECHSTETTER L,
ET AL: Gastrointestinal transit time: The effect of the menstrual cycle. Gastroenterology 80:1497-1500,1981
LUBA GARBACZEWSKI
Rockefeller University New York, NY
JHH,
ET AL: Fat, gut-CNS peptide hormones and breast cancer. Presented at the American Association of Cancer Research Meeting, Atlanta, GA, March 20-23, 1987 (5) DREWNOWSKI A: Food perceptions and preferences in obese adults. A multidimensional approach. Int J Obes 9:201-212, 1985
(13)
HOLST N, JENSSEN TG, BURHOL PG, ET AL:
Plasma gastrointestinal hormones during spontaneous and induced menstrual cycles. J Clin Endocrinol Metab 68:1160-1166, 1989 (14) HOGSTON P: Irritable bowel syndrome as a cause of chronic pain in women attending a gynecological clinic. Br Med J [Clin Res] 294:934-935, 1987 (15) GUTHRIE E, CREED FH, WHORWELL PJ:
Se-
vere sexual dysfunction in women with irritable bowel syndrome: Comparison with inflammatory bowel disease and duodenal ulceration. Br Med J [Clin Res] 295:577578, 1987 (16)
HILL P, THUSSEN JHH,
BARBACZEWSKI L,
ET AL: VIP and prolactin release in response to meals. Scand J Gastroenterol 21:958-960, 1986 (17) HILL P: Diet and plasma prolactin. Am J Clin Nutr 34:1162-1163, 1981
Journal of the National Cancer Institute
Downloaded from http://jnci.oxfordjournals.org/ at Harvard University on July 11, 2015
matched control subjects. In the control subjects, the opioid status is modified by environmental factors. The opioid peptide hormones have the following functions; a) enhance food intake, b) tonic inhibition of luteinizing hormonereleasing hormone-luteinizing hormone release, c) inhibitory action on the GI tract. Therefore, we determined the effect of administration of naloxone, an opioid peptide antagonist, on the GI peptide hormone response to a fat meal. In addition, because lean and obese women have different dietary preferences (5), we determined the effect of cholecystokinin on the GI peptide hormone response. Published studies show a different GI peptide honnone response in lean and obese women to a fat meal. The GI peptide honnone response to naloxone and cholecystokinin administration was different in lean and obese women (6-8).
Department of Cellular and Structural Biology The University of Texas Health Science Center San Antonio, Tex
( / / ) FREEMAN HJ, SPILLER GA, KIM YS: A dou-
ble-blind study on the effects of differing purified cellulose and pectin fiber diets on 1,2-dimethylhydrazine-induced rat colonic neoplasia. Cancer Res 40:2661-2665, 1980 (12) HHTMAN DW, ORD VA, HUNTER KE, ET AL:
Effect of dietary cellulose on cell proliferation and progression of 1,2-dimethylhydrazineinduced colon carcinogenesis in rats. Cancel Res 49:5581-5585, 1989 (13) LJPKIN M: Biomarkers of increased susceptibility of gastrointestinal cancer. Their development and application to studies of cancer prevention. Gastroenterology 92:1083-1086, 1987 (14) LJPKIN M: Biomarkers of increased susceptibility to gastrointestinal cancer. New application to studies of cancer prevention in human subjects. Cancer Res 48:235-245, 1988 (15) COLE JW, MCKALEN A: Studies on the mor-
References
phogenesis of adenomatous polyps in the human colon. Cancer 16:998-1002, 1963 (16) DESCHNER EE, LEWIS CM, LJPKIN M: In vitro
(/) DECOSSE JJ, MILLER HH, LESSER ML: Effect
(6) NATIONAL ACADEMY OF SCIENCE, NATIONAL
RESEARCH COUNCIL: Diet, Nutrition, and
Cancer. Washington, DC: National Academy Press, 1982 (7) JACOBS LR, LUPTON JR: Relationship be-
tween colonic Iuminal pH, cell proliferation, and colon carcinogenesis in 1,2-dimethylhydrazine-treated rats fed high fiber diets. Cancer Res 46:1727-1734, 1986 (8) FREEMAN HJ, SPILLER GA, KIM YS: A dou-
ble-blind study on the effect of purified cellulose dietary fiber on 1,2-dimethylhydrazineinduced rat colonic neoplasia. Cancer Res 38:2912-2917, 1978 (9) BAUER HG, ASP NG, OSTER.ETAL: Effect of
dietary fiber on the induction of colorectal tumors and fecal fj-glucuronidase activity in the rat. Cancer Res 39:3752-3756, 1979 (70) NIGRO ND, BULL SW, KLOPFER BA, ET AL:
Effect of dietary fiber on azoxymethane-induced intestinal carcinogenesis in rats. JNCI 62:1097-1102,1979
Vol. 82, No. 13, July 4, 1990
Reference (/) DECOSSE JJ, MILLER HH, LESSER ML: Effect
of wheat fiber and vitamins C and E on rectal polyps in patients with familial adenomatous polyposis. J Natl Cancer Inst 81:1290-1297, 1989
study of human epithelial cells. I. Atypical zone of H3-thymidine incorporation in mucosa of multiple polyposis. J Clin Invest 42:1922-1928, 1963 (17) DESCHNER EE, LJPKIN M, SOLOMON C: Study
of human rectal epithelial cells in vitro. U. H3-thymidine incorporation into polyps and adjacent mucosa. J Natl Cancer Inst 36:849-857, 1966
Response
(5) ROGERS AE, NAUS KM: Contributions of
laboratory animal studies of colon carcinogenesis. In Large Bowel Cancer (Mastromarino AJ, Brattain MG, eds). New York: Praeger, 1984, pp 1-45
JEROME J. DECOSSE
Department of Surgery (F-1917) The New York HospitalCornell Medical Center 525 E. 68th St. New York, NY 10021
Drs. Heitman and Cameron address our recent article (7) in which we reported that a wheat bran supplement in excess of 11 g/day was associated with regression of rectal polyps in patients with familial adenomatous polyposis. The gist of their letter is that cellulose is the effective component of insoluble fiber and that human trials should now be initiated with cellulose. The data provided on cellulose are interesting and, indeed, trials of insoluble fiber need to be initiated in patients with an average risk of colon cancer. However, as a fundamental strategy in extending a study, one should go with what seems to work, namely, wheat bran, not one of its components. Moreover, in a long-term study that may extend beyond 5 years, the palatability of the treatment agent is critically important. Developing a reliably palatable form of cellulose would be a prerequisite for a cellulose trial. Finally, studies in
Gastrointestinal Peptide Hormones and Breast Cancer The recent paper by Goettler et al. (7) raises the issue of whether changes in gastrointestinal (GI) response are predisposing factors in the development of breast cancer. As noted by Goettler et al., we have reported a higher release of gastrin, but no release of vasoactive intestinal polypeptide or neurotensin in premenopausal patients with breast cancer (2-4). However, a number of conditions are related to such data. Initially, we compared the GI peptide hormone response to isocaloric carbohydrate or "fat" breakfasts in three groups of healthy premenopausal women, body mass index less than 23, 24-27, or more than 28, and in women with stage LT breast cancer to age- and weight-
Downloaded from http://jnci.oxfordjournals.org/ at Harvard University on July 11, 2015
of wheat fiber and vitamins C and E on rectal polyps in patients with familial adenomatous polyposis. J Natl Cancer Inst 81:1290-1297, 1989 (2) JACOBS LR: Enhancement of rat colon carcinogenesis by wheat bran consumption during the stage of 1,2-dimethylhydrazine administration. Cancer Res 43:4057-4061, 1983 (3) ZARIDZE DG: Environmental etiology of large-bowel cancer. JNCI 70:389^00, 1983 (4) WnxETT WC, MACMAHON B: Diet and cancer—an overview. I and D. N Engl J Med 310:633-^38,697-703,1984
patients with an average risk of colon cancer must also recognize the potential importance of a low-fat diet in risk reduction.
*Correspondence to: Peter Hill, Ph.D., Mahoney Institute, American Health Foundation, 320 E. 43rd St., New York, NY 10017.
CORRESPONDENCE 1155
As reported by Goettler et al. (7) in postmenopausal patients, we reported a higher gastrin release in premenopausal patients after a fat meal than in the ageand weight-matched control subjects. The increase in plasma vasoactive intestinal polypeptide in the control group after a fat meal was not found in patients with breast cancer (3). No increase in vasoactive intestinal polypeptide occurred after a carbohydrate meal in the control group. While these findings are ostensibly similar to those of Goettler et al. (7), the difference in response due to the effects of body mass index or administration of naloxone or cholecystokinin evident between lean women with a body mass index that was less than 23 and obese women with a body mass index greater than 28, implies a difference in their physiological status. Overlapping responses occurred in women whose body mass index was 24-27 (7). This finding applied to our observations in age- and weight-matched controls with a body mass index of 24.7 ± 0.73 and could apply to the results obtained by Goettler etal. (7). This problem applies to neurotensin release in response to naloxone and cholecystokinin, where cholecystokinin suppresses neurotensin release only in obese women, body mass index greater than 28, while naloxone suppresses neurotensin release in lean women, but in-
1156
creases neurotensin release in obese women (2,6). Since behavioral stress affects digestion (9,70), differences in GI response can be modified in patients, leading to anomalies such as an unexpected weight gain in some premenopausal patients receiving chemotherapy. It is of interest that gastrin and vasoactive intestinal polypeptide responses to a fat meal are similar in premenopausal and postmenopausal patients since gonadal steroids not only affect a number of central nervous system peptide hormones, opioids, neuropeptide Y, and substance P (peptide hormones associated with digestion and release of luteinizing hormone-releasing hormone-luteinizing hormone release), but also food intake (77), GI transit time (72), and GI peptide hormone release (13). Although a high frequency of concomitant gynecologic and digestive dysfunction (14,15) does not prove causality, a common gonadal honnone dysfunction is suggested in these patients. We concur with Goettler et al. (7) that changes in prolactin metabolism are predominantly related to protein (16,17). Accordingly, the findings of Goettler et al. and our data indicate a previously neglected step between luminal nutrients and circulating nutrients that may play a major role in controlling differentiation of growth factors in diet-hormone-related diseases. PETER HILL*
Mahoney Institute American Health Foundation New York, NY
References (1) GOETTLER DM, LEVINE L, CHEY WY: Post-
prandial levels of prolactin and gut hormones in breast cancer patients: Association with stage of disease, but not dietary fat. J Nat! Cancer Inst 82:22-28, 1990 (2) KOPPESCHAAR HPP, HILL P, GARBACZEWSKI
L, ET AL: Effect of meals, naloxone and cholecystokinin on plasma neurotensin levels in lean and obese women. Presented at the 4th International Congress on Obesity, Stockholm, Sweden, June 1989 (3) Hm. P, DE WAARD F, THUSSEN JHH, ET AL:
Gut-CNS peptide hormones in healthy women and breast cancer patients. Presented at the 3rd Annual European Cancer Prevention Symposium, Aarhus, Denmark, 1985 (4) HEX P, GARBACZEWSKI L, THUSSEN
(6) HILL P, GARBACZEWSKI L, KOOPESCHAAR
HPP, ET AL: Peptide hormones, digestion and menstrual periodicity. In The Menstrual Cycle and Its Disorders (Pirke KM, Luuttke K, Schweiger V, eds). Berlin: Springer-Verlag, 1989, pp 133-141 (7) HILL P,
Jos H. H. THUSSEN
HANS KOPPERSCHAAR
Department of Endocrinology Utrecht University Hospital Utrecht, The Netherlands
GARBACZEWSKI L, KOPPESCHAAR
HPP, ET AL: Glucagon and insulin response to meals in non-obese and obese Dutch women. ClinChim Acta 165:253-263, 1987 (8) HILL P,
GARBACZEWSKI L, KOPPESCHAAR
HPP, ET AL: Peptides and steroid hormones in subjects at different risk for diet-related diseases. Am J Clin Nutr 48:782-786, 1988 (9) WELOAN P, MESHKINPOUR H, BEELER M:
Effect of anger on colon motor and myoelectric activity in irritable bowel syndrome. Gastroenterology 94:1150-1156, 1988 (10) HOLTMANNG,SINGERMV.KREIBELR,ETAL:
Differential effects of acute mental stress on interdigestive secretion of gastric acid, pancreatic enzymes and gastroduodenal motility. Dig Dis Sci 34:1701-1707, 1989 (11) DALVTT SP: The effect of the menstrual cycle on patterns of food intake. Am J Clin Nutr 34:1811-1815,1981 (12) WALD A, VAN THIEL DH, HOECHSTETTER L,
ET AL: Gastrointestinal transit time: The effect of the menstrual cycle. Gastroenterology 80:1497-1500,1981
LUBA GARBACZEWSKI
Rockefeller University New York, NY
JHH,
ET AL: Fat, gut-CNS peptide hormones and breast cancer. Presented at the American Association of Cancer Research Meeting, Atlanta, GA, March 20-23, 1987 (5) DREWNOWSKI A: Food perceptions and preferences in obese adults. A multidimensional approach. Int J Obes 9:201-212, 1985
(13)
HOLST N, JENSSEN TG, BURHOL PG, ET AL:
Plasma gastrointestinal hormones during spontaneous and induced menstrual cycles. J Clin Endocrinol Metab 68:1160-1166, 1989 (14) HOGSTON P: Irritable bowel syndrome as a cause of chronic pain in women attending a gynecological clinic. Br Med J [Clin Res] 294:934-935, 1987 (15) GUTHRIE E, CREED FH, WHORWELL PJ:
Se-
vere sexual dysfunction in women with irritable bowel syndrome: Comparison with inflammatory bowel disease and duodenal ulceration. Br Med J [Clin Res] 295:577578, 1987 (16)
HILL P, THUSSEN JHH,
BARBACZEWSKI L,
ET AL: VIP and prolactin release in response to meals. Scand J Gastroenterol 21:958-960, 1986 (17) HILL P: Diet and plasma prolactin. Am J Clin Nutr 34:1162-1163, 1981
Journal of the National Cancer Institute
Downloaded from http://jnci.oxfordjournals.org/ at Harvard University on July 11, 2015
matched control subjects. In the control subjects, the opioid status is modified by environmental factors. The opioid peptide hormones have the following functions; a) enhance food intake, b) tonic inhibition of luteinizing hormonereleasing hormone-luteinizing hormone release, c) inhibitory action on the GI tract. Therefore, we determined the effect of administration of naloxone, an opioid peptide antagonist, on the GI peptide hormone response to a fat meal. In addition, because lean and obese women have different dietary preferences (5), we determined the effect of cholecystokinin on the GI peptide hormone response. Published studies show a different GI peptide honnone response in lean and obese women to a fat meal. The GI peptide honnone response to naloxone and cholecystokinin administration was different in lean and obese women (6-8).
