Amino Acids

, Volume 42, Issue 4, pp 1397–1404

Somatostatin is involved in anorexia in mice fed a valine-deficient diet

Authors

  • Keiko Nakahara
    • Department of Veterinary Physiology, Faculty of AgricultureUniversity of Miyazaki
  • Shiori Takata
    • Department of Veterinary Physiology, Faculty of AgricultureUniversity of Miyazaki
  • Asami Ishii
    • Department of Veterinary Physiology, Faculty of AgricultureUniversity of Miyazaki
  • Kenji Nagao
    • Frontier Research Labs, Institute For Innovation, Ajinomoto Co., Inc.
  • Makoto Bannai
    • Frontier Research Labs, Institute For Innovation, Ajinomoto Co., Inc.
  • Michio Takahashi
    • Frontier Research Labs, Institute For Innovation, Ajinomoto Co., Inc.
    • Department of Veterinary Physiology, Faculty of AgricultureUniversity of Miyazaki
Original Article

DOI: 10.1007/s00726-011-0836-z

Cite this article as:
Nakahara, K., Takata, S., Ishii, A. et al. Amino Acids (2012) 42: 1397. doi:10.1007/s00726-011-0836-z

Abstract

The ingestion of a valine (Val)-deficient diet results in a significant reduction of food intake and body weight within 24 h, and this phenomenon continues throughout the period over which such a diet is supplied. Both microarray and real-time PCR analyses revealed that the expression of somatostatin mRNA was increased in the hypothalamus in anorectic mice that received a Val-deficient diet. On the other hand, when somatostatin was administered intracerebroventricularly to intact animals that were fed a control diet, their 24-h food intake decreased significantly. In addition, Val-deficient but not pair-fed mice or those fasted for 24 h showed a less than 0.5-fold decrease in the hypothalamic mRNA expression levels of Crym, Foxg1, Itpka and two unknown EST clone genes and a more than twofold increase in those of Slc6a3, Bdh1, Ptgr2 and one unknown EST clone gene. These results suggest that hypothalamic somatostatin and genes responsive to Val deficiency may be involved in the central mechanism of anorexia induced by a Val-deficient diet.

Keywords

Amino acid deficiency Valine Anorexia nervosa Somatostatin

Supplementary material

726_2011_836_MOESM1_ESM.tif (114 kb)
Fig. s1 Quantitative analysis of the levels of expression of somatostatin mRNA in the hypothalamus of mice that received the standard diet (control) and the Val-deficient diet. In the Val-deficient groups, hypothalamic samples were collected at 6, 12, 24, 48 and 72 h after switching from the control to the Val-deficient diet, and 5 days after switching back from the Val-deficient to the standard diet. Data represent the mean ± SEM. Asterisks indicate significant differences vs. the control group (*P < 0.05). (TIFF 113 kb)
726_2011_836_MOESM2_ESM.tif (106 kb)
Fig. s2: Effect of icv injection of somatostatin on food intake in rats. Adult male Wistar rats received an implanted intracerebroventricular stainless steel cannula, and four days later, somatostatin (at doses of 0.1, 0.5, 1.5 nmol/10 μl) was injected at 18:30 h, and then the 24-h food intake was measured. All data represent the mean ± SEM. Asterisks indicate significant differences vs. the control group (*P < 0.05). (TIFF 105 kb)
726_2011_836_MOESM3_ESM.tif (1.1 mb)
Fig. s3: Although we were unable to confirm the data by real-time PCR, microarray analysis showed that the expression levels of the Sgk1, Pdk4, Arl4d, S3-12, Cdkn1a, Sulta1, Ddit4, Arrdc2, 6030422H21Rik, 1810011O10Rik and Nfkbia genes were more than 2-fold higher, and that the expression levels of the Gm1337, Arpp21, Pitpnm3 and Atp8b1 genes showed a difference of less than 0.5-fold in the Val-deficient, pair-fed and 24-h-fasted groups in comparison with the control group. (TIFF 1172 kb)

Copyright information

© Springer-Verlag 2011