{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,10]],"date-time":"2025-10-10T01:54:56Z","timestamp":1760061296427,"version":"build-2065373602"},"reference-count":59,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2008,11,27]],"date-time":"2008-11-27T00:00:00Z","timestamp":1227744000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cell Biochemistry &amp;amp; Function"],"published-print":{"date-parts":[[2008,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Type 2 diabetes is associated with obesity, insulin resistance, hyperglycemia, hyperphagia, polyuria, body weight gain, excessive secretion of glucocorticoids (GCs), thymus involution, adrenal gland hypertrophy, diabetic nephropathy, etc. We examined the effect of cerebrocrast, a new antidiabetic agent (synthesized in the Latvian Institute of Organic Synthesis), on body weight, food and water intake, urine output, and on changes of organ weight: that is, kidney, thymus, adrenal gland of normal rats. Cerebrocrast was administered at doses of 0.05 and 0.5\u2009mg\u2009kg<jats:sup>\u22121<\/jats:sup> <jats:italic>per os<\/jats:italic> (p.o.) once a day for three consecutive days, and its effects were observed from 3 to 27 days after the last administration. Cerebrocrast, during the experimental period, decreased body weight by an average of approximately 32.3%, food intake by about 10\u201315% at the beginning of the experiments and by 22.6% at the end of the experiments, especially at a dose of 0.5\u2009mg\u2009kg<jats:sup>\u22121<\/jats:sup>. Water intake and urine output in comparison with controls were decreased. The daily food intake decreased about 1.0 and 2.1\u2009g by administering single cerebrocrast doses of 0.05 and 0.5\u2009mg\u2009kg<jats:sup>\u22121<\/jats:sup> body weight (b.w.), respectively, but by administering for three consecutive days, food intake decreased by about 2.2 and 3.4\u2009g, respectively. The weekly body weight gain decreased by administering a single dose of cerebrocrast by 2.61 and 2.51\u2009g, respectively, and by triple administration it decreased by 4.36 and 3.07\u2009g, respectively. Cerebrocrast has long\u2010lasting effects on these parameters and on thymus and adrenal gland weight. As cerebrocrast decreased glucose levels in normal and streptozotocin (STZ)\u2010induced diabetic rats, it also promoted glucose uptake by the brain, intensified insulin action and formation <jats:italic>de novo<\/jats:italic> of insulin receptors. We can conclude that cerebrocrast may regulate food intake and body weight through glucose sensing by proopiomelanocortin (POMC) neurons, that are involved in control of glucose homeostasis, stimulation of <jats:italic>\u03b1<\/jats:italic>\u2010melanocyte\u2010stimulating hormone (<jats:italic>\u03b1<\/jats:italic>\u2010MSH) secretion, activation of MC4\u2010Rs and inhibition of neuropeptide Y (NPY) in the ARC of the hypothalamus, affecting the kidney, and causing decreased urine output and water intake. Moreover, it could stimulate secretion of vasopressin. By administration of cerebrocrast thymus mass was increased, thereby preventing the action of GCs. As cerebrocrast inhibited L\u2010 and T\u2010type calcium channels, it can prevent vasoconstriction of kidney arterioles and aldosterone secretion that have significant roles in the development of hypertension and diabetic nephropathy. These properties of cerebrocrast are important for treatment of Type 2 diabetes and its consequent development of hypertension and diabetic nephropathy. Copyright \u00a9 2008 John Wiley &amp; Sons, Ltd.<\/jats:p>","DOI":"10.1002\/cbf.1525","type":"journal-article","created":{"date-parts":[[2008,11,27]],"date-time":"2008-11-27T11:09:35Z","timestamp":1227784175000},"page":"908-915","source":"Crossref","is-referenced-by-count":4,"title":["Effect of cerebrocrast on body and organ weights, food and water intake, and urine output of normal rats"],"prefix":"10.1002","volume":"26","author":[{"given":"Janina","family":"Briede","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mara","family":"Stivrina","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dzintra","family":"Stoldere","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brigita","family":"Vigante","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gunars","family":"Duburs","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2008,11,27]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.18.10397"},{"key":"e_1_2_1_3_2","first-page":"213","article-title":"Vasopressin and urinary concentrating activity in diabetes mellitus","volume":"25","author":"Ahloulay M","year":"1999","journal-title":"Diabete Metab"},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2826.1996.05124.x"},{"key":"e_1_2_1_5_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00214.2004"},{"key":"e_1_2_1_6_2","doi-asserted-by":"crossref","first-page":"9","DOI":"10.1161\/01.HYP.0000151325.83008.b4","article-title":"Obesity\u2010associated hypertension. 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