The pineal gland of the chick is composed of vesicles during much of the incubation period. During incubation, these vesicles increase in size and number and reach maximum development at the 17-day prehatching stage. After day 17, the vesicular tissue decreases and, by 1 day posthatching, only a few vesicles remain. All vesicles have disappeared by 1 month posthatching and the gland has acquired a compact, lobed character. The vesicular cells are secretory in nature and react positively with tests for glycogen, glycoproteins, ribonucleic acid, acid mucopolysaccharides, and neutral lipids. In addition, the specialized apical border of these cells stains intensely for acid lipids. The vesicles contain a secretory product which includes a sulfated mucopolysaccharide component. Based on the intensities of the staining reactions, this secretion is present in greatest amounts during the 15- to 17-day prehatching period. No secretory product could be demonstrated after 1 day posthatching. It appears, therefore, that the development of the vesicular tissue is related to some secretory role and that this role is culminated during the 15- to 17-day prehatching period. After day 17, the decrease and eventual disappearance of the vesicles apparently marks the conclusion of this secretory phase for the gland.

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It has been known for years that free access to sugar solutions can cause weight gain and/or obesity in rats. We recently reported that brief access to sugar solutions can affect the hypothalamic neuropeptides that help to regulate energy balance. In this paper, we present the results in which we examined the effects of these sugars on the expression of several neuropeptides within specific hypothalamic regions. We provided Sprague Dawley rats 24 h access to 15% solutions of glucose, fructose, sucrose or high fructose corn syrup (HFCS) and then dissected portions of the paraventricular hypothalamic nuclei (PVN), the ventromedial hypothalamus (VMH) and the lateral hypothalamus (LH). We then evaluated the expression of several neuropeptides in these tissues, all of which were previously shown to be influenced by free access to sugar solutions using PCR array. Of the four sugar solutions tested, only fructose decreased expression of cholecystokinin (CCK) significantly, and only in the PVN. Glucose and sucrose significantly increased the expression of Tumor Necrosis Factor α (TNF-α) only in the PVN. Fructose and sucrose decreased Growth Hormone (GH) in the VMH. Further analysis indicated that it was fructose intake that was negatively correlated with both CCK and GH expression. Rats that had access to sugar solutions consumed less chow but maintained control levels of total caloric intake. We conclude that 24 h free access to different sugars can influence the expression of several hypothalamic neuropeptides in different ways. Changes in the expression of these neuropeptides do not disrupt total daily energy intake immediately but may nevertheless contribute to the obesity caused by long term access to sugar solutions.

Fructose consumption can promote hypertriglyceridemia (HTG) in both humans and laboratory animals. We have recently reported that giving rats overnight access to a 16% fructose solution results in HTG. Several investigators have suggested that hepatic FOXO1 and/or APOC 3 may be implicated in promoting fructose‐induced HTG. We have found that neither FOXO1 nor APOC 3 expression in the livers of rats fed fructose differed from controls that were fed lab chow only. Similarly, neither FOXO1 nor APOC 3 expression in rats fed glucose, sucrose or high fructose corn syrup solutions were significantly different from controls. These results suggest that the changes in FOXO1 and APOC 3 following fructose consumption are secondary to the changes necessary to cause fructose‐induced HTG. Alternatively, hepatic FOXO1 and/or APOC 3 expression may have been returned to pre‐fructose levels prior to sampling. In future experiments we intend to monitor postprandial hepatic expression of FOX01 and APOC 3 in hourly intervals to better characterize the onset of HTG. Supported in part by a grant from the Maryland Agricultural Experiment Station.

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