Neurosecretory Protein GL Induces Fat Accumulation in Chicks.

We recently found a previously unidentified cDNA in chicken hypothalamus which encodes the precursor for neurosecretory protein GL (NPGL). A previous study showed that intracerebroventricular (i.c.v.) infusion of NPGL caused body mass gain in chicks. However, it was not clear which part(s) of the body gained mass. In the present study, we investigated which tissues increased in mass after chronic i.c.v. infusion of NPGL in chicks. We found that NPGL increased the masses of the liver, abdominal fat, and subcutaneous fat, while NPGL did not affect the masses of muscles, including pectoralis major, pectoralis minor, and biceps femoris. Oil Red O staining revealed that fat deposition had occurred in the liver. In addition, the size of the lipid droplets in the abdominal fat increased. Furthermore, we found an upregulation of lipogenesis and downregulation of lipolysis in the abdominal fat, but not in the liver. These results indicate that NPGL is involved in fat storage in chicks

Neurosecretory protein GL stimulates food intake, de novo lipogenesis, and onset of obesity.

Mechanisms underlying the central regulation of food intake and fat accumulation are not fully understood. We found that neurosecretory protein GL (NPGL), a newly-identified neuropeptide, increased food intake and white adipose tissue (WAT) in rats. NPGL-precursor gene overexpression in the hypothalamus caused increases in food intake, WAT, body mass, and circulating insulin when fed a high calorie diet. Intracerebroventricular administration of NPGL induced de novo lipogenesis in WAT, increased insulin, and it selectively induced carbohydrate intake. Neutralizing antibody administration decreased the size of lipid droplets in WAT. Npgl mRNA expression was upregulated by fasting and low insulin levels. Additionally, NPGL-producing cells were responsive to insulin. These results point to NPGL as a novel neuronal regulator that drives food intake and fat deposition through de novo lipogenesis and acts to maintain steady-state fat level in concert with insulin. Dysregulation of NPGL may be a root cause of obesity

Neurosecretory Protein GL Induces Fat Accumulation in Chicks.

We recently found a previously unidentified cDNA in chicken hypothalamus which encodes the precursor for neurosecretory protein GL (NPGL). A previous study showed that intracerebroventricular (i.c.v.) infusion of NPGL caused body mass gain in chicks. However, it was not clear which part(s) of the body gained mass. In the present study, we investigated which tissues increased in mass after chronic i.c.v. infusion of NPGL in chicks. We found that NPGL increased the masses of the liver, abdominal fat, and subcutaneous fat, while NPGL did not affect the masses of muscles, including pectoralis major, pectoralis minor, and biceps femoris. Oil Red O staining revealed that fat deposition had occurred in the liver. In addition, the size of the lipid droplets in the abdominal fat increased. Furthermore, we found an upregulation of lipogenesis and downregulation of lipolysis in the abdominal fat, but not in the liver. These results indicate that NPGL is involved in fat storage in chicks

Author Correction: Localization and function of neurosecretory protein GM, a novel small secretory protein, in the chicken hypothalamus

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has not been fixed in the paper

Author Correction: Localization and function of neurosecretory protein GM, a novel small secretory protein, in the chicken hypothalamus.

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has not been fixed in the paper

Localization and function of neurosecretory protein GM, a novel small secretory protein, in the chicken hypothalamus.

Recently, we discovered a novel cDNA encoding the precursor of a small secretory protein, neurosecretory protein GL (NPGL), in the hypothalamic infundibulum of chickens. NPGL plays an important role in the regulation of growth and feeding. A database search indicated that the NPGL gene has a paralogous gene: neurosecretory protein GM (NPGM), also in chickens. We identified cDNA encoding the NPGM precursor in chickens. Morphological analysis showed that NPGM-containing cells are specifically localized in the medial mammillary nucleus (MM) and infundibular nucleus (IN) in the hypothalamus. In addition, we found that NPGM and NPGL are co-localized, especially in the MM. The expression levels of NPGM mRNA gradually decreased during post-hatch development, in contrast to those of NPGL mRNA. Moreover, we investigated the relationship between NPGM and other known factors. NPGM was found to be produced in histaminergic neurons in the MM. NPGM and histidine decarboxylase, a histamine-producing enzyme, displayed similar expression patterns during post-hatch development. Acute intracerebroventricular injection of NPGM decreased food intake, similar to the effect of histamine. To our knowledge, this is the first report of the localization and function of NPGM in the brain of vertebrates. These results will further advance the understanding mechanisms underlying energy homeostasis

Impact of Chronic Prenatal Stress on Maternal Neuroendocrine Function and Embryo and Placenta Development During Early-to-Mid-Pregnancy in Mice

Psychological stress, both leading up to and during pregnancy, is associated with increased risk for negative pregnancy outcomes. Although the neuroendocrine circuits that link the stress response to reduced sexual motivation and mating are well-described, the specific pathways by which stress negatively impacts gestational outcomes remain unclear. Using a mouse model of chronic psychological stress during pregnancy, we investigated 1) how chronic exposure to stress during gestation impacts maternal reproductive neuroendocrine circuitry, and 2) whether stress alters developmental outcomes for the fetus or placenta by mid-pregnancy. Focusing on the stress-responsive neuropeptide RFRP-3, we identified novel contacts between RFRP-3-immunoreactive (RFRP-3-ir) cells and tuberoinfundibular dopaminergic neurons in the arcuate nucleus, thus providing a potential pathway linking the neuroendocrine stress response directly to pituitary prolactin production and release. However, neither of these cell populations nor circulating levels of pituitary hormones were affected by chronic stress. Conversely, circulating levels of steroid hormones relevant to gestational outcomes (progesterone and corticosterone) were altered in chronically-stressed dams across gestation, and those dams were qualitatively more likely to experience delays in fetal development. Together, these findings suggest that, up until at least mid-pregnancy, mothers appear to be relatively resilient to the effects of elevated glucocorticoids on reproductive neuroendocrine system function. We conclude that understanding how chronic psychological stress impacts reproductive outcomes will require understanding individual susceptibility and identifying reliable neuroendocrine changes resulting from gestational stress