Sexually dimorphic expression of prepro-orexin mRNA in the rat hypothalamus

Jöhren, Olaf; Neidert, Steffi J.; Kummer, Marco; Dominiak, Peter

doi:10.1016/s0196-9781(02)00052-9

Cited by 94 publications

(56 citation statements)

References 30 publications

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“…The levels are low up to day 15, and then increases between days 15 and 20, when expression levels achieve values similar to those found during adulthood (Yamamoto et al, 2000a). In adults, there are sexual dimorphic differences in prepro-OX mRNA expression, with higher levels in females, thus suggesting gender-specific functions of orexins (Johren et al, 2002).…”

Section: Anatomy Of the Orexin/hypocretin Systemsupporting

confidence: 54%

Orexins (hypocretins) and energy balance: More than feeding

Fernø

Señarı́s

Diéguez

et al. 2015

Molecular and Cellular Endocrinology

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Section: Anatomy Of the Orexin/hypocretin Systemsupporting

confidence: 54%

Orexins (hypocretins) and energy balance: More than feeding

Fernø

Señarı́s

Diéguez

et al. 2015

Molecular and Cellular Endocrinology

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“…The leptin levels are influenced by various hormones and cytokines that are also under the influence of gender [3,14], and leptin levels in females are higher than in males [3,8,14]. Similarly, higher levels of preprohypocretin mRNA in the hypothalamus of female rats compared to male rats are reported [15]. As mentioned earlier, leptin significantly affects hypocretin signaling [29].…”

Section: Discussionmentioning

confidence: 99%

Sex difference in body weight gain and leptin signaling in hypocretin/orexin deficient mouse models

Fujiki

Yoshida²,

Zhang³

et al. 2006

Peptides

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Recent studies in human and animal models of narcolepsy have suggested that obesity in narcolepsy may be due to deficiency of hypocretin signaling, and is also under the influence of environmental factors and the genetic background. In the current study, using two hypocretin/orexin deficient narcoleptic mouse models (i.e. prepro-orexin knockout (KO) and orexin/ataxin-3 transgenic (TG) mice) with cross-sectional assessments, we have further analyzed factors affecting obesity. We found that both KO and TG narcoleptic mice with mixed genetic backgrounds (N4-5, 93.75-96.88 % genetic composition of C57BL/6) tended to be heavier than wild type (WT) mice of 100 to 200 days old. The body weight of heterozygous mice was intermediate between those of KO and WT mice. Obesity was more prominent in females in both KO and TG narcoleptic mice and was associated with higher serum leptin levels, suggesting a partial leptin resistance. Obesity is less prominent in the congenic TG narcoleptic mice, but is still evident in females. Our results confirmed that hypocretin/orexin ligand deficiency is one of the critical factors for the obese tendency in narcolepsy. However, multiple factors are also likely to affect this phenotype, and a gender specific alteration of leptin-hypocretin signaling may be involved.

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“…Section 5) (Schmitt et al, 2012). What makes this system especially interesting in the context of PD that within the hypothalamus, expression of the mRNA encoding for prepro-ORX (ORX precursor) measured in females is higher than males (Jöhren et al, 2002) and expression of OX 1 receptors is influenced by gonadal steroids (Silveyra et al, 2009). Furthermore, ORX neurons were recently shown to exhibit CO 2 /H + sensing properties.…”

Section: Orexinergic Neurons Of the Dorso-medial/perifornical Hypothamentioning

confidence: 99%