Feeding and hyperglycemia induced by 1,5-anhydroglucitol in the rat

Sakata, Toshiie; Tsutsui, Koichiro; Fukushima, Masataka; Arase, Koichi; Kita, Hitoshi; Osuga, Yutaka; Ohki, Kosuke; Nicolaı̈dis, Stylianos

doi:10.1016/0031-9384(81)90323-1

Cited by 46 publications

(13 citation statements)

References 18 publications

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“…A 23-gauge 15-mm-long stainless steel cannula was inserted into the third ventricle at the midline 6.0 mm anterior to ear bar zero to a depth of 7.8 mm from the cortical surface, according to the atlas of Paxinos and Watson (18). Details of the surgical procedure have been described previously (19).…”

Section: Surgerymentioning

confidence: 99%

Glucagon‐like peptide‐1, corticotropin‐releasing hormone, and hypothalamic neuronal histamine interact in the leptin‐signaling pathway to regulate feeding behavior

Gotoh

Fukagawa

et al. 2005

FASEB j.

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Glucagon-like peptide-1 (GLP-1), corticotropin-releasing hormone (CRH), and hypothalamic neuronal histamine suppress food intake, a target of leptin action in the brain. This study examined the interactions of GLP-1, CRH, and histamine downstream from the leptin-signaling pathway in regulating feeding behavior. Infusion of GLP-1 into the third cerebral ventricle (i3vt) at a dose of 1 mug significantly decreased the initial 1 h cumulative food intake in rats as compared with phosphate-buffered saline (PBS) controls. The GLP-1-induced suppression of feeding was partially attenuated by intraperitoneal pretreatment with alpha-fluoromethylhistidine (FMH), a specific suicide inhibitor of histidine decarboxylase, which depletes hypothalamic neuronal histamine. Pretreatment with alpha-helical CRH (10 microg/rat, i3vt), a nonselective CRH antagonist, abolished the GLP-1-induced suppression of feeding completely. I3vt infusion of GLP-1 increased the CRH content and histamine turnover assessed using the pargyline-induced accumulation of tele-methyl histamine (t-MH), a major metabolite of neuronal histamine, in the hypothalamus. The central infusion of CRH also induced the increase of histamine turnover and CRH receptor type 1 was localized on the cell body of histamine neuron. Pretreatment with exendin(9-39), a GLP-1 receptor antagonist, attenuated the leptin-induced increase in CRH content of the hypothalamus. Finally, i3vt infusion of leptin also increased histamine turnover in the hypothalamus. Pretreatment with exendin(9-39), alpha-helical CRH or both antagonists attenuated the leptin-induced responses of t-MH levels in the hypothalamus. These results suggest that CRH or hypothalamic neuronal histamine mediates the GLP-1-induced suppression of feeding behavior, that CRH mediates GLP-1 signaling to neuronal histamine and that a functional link from GLP-1 to neuronal histamine via CRH constitutes the leptin-signaling pathway regulating feeding behavior.

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Section: Surgerymentioning

confidence: 99%

Glucagon‐like peptide‐1, corticotropin‐releasing hormone, and hypothalamic neuronal histamine interact in the leptin‐signaling pathway to regulate feeding behavior

Gotoh

Fukagawa

et al. 2005

FASEB j.

Self Cite

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“…t‐MH contents were assayed via HPLC, using the deproteinized supernatants containing the amine extracts. The details of amine assays have been described elsewhere (Sakata et al. 1981).…”

Section: Methodsmentioning

confidence: 99%

Hypothalamic neuronal histamine signaling in the estrogen deficiency‐induced obesity

Gotoh

Masaki

Chiba

et al. 2009

Journal of Neurochemistry

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Menopause is one of the triggers that induce a variety of agerelated diseases such as osteoporosis, atherosclerosis, and obesity (Genazzani and Gambacciani 2001). The incidence of obesity is higher in post-menopausal women than in agematched pre-menopausal women; this increase is thought to be associated with the decline of estrogen levels after menopause. In fact, estrogen replacement therapy is an effective treatment to reduce body weight and fat accumulation in post-menopausal women (Svendsen et al. 1995). In rats, estrogen treatment reduces energy intake (Donohoe and Stevens 1983), and it has been demonstrated that ovariectomy (OVX) induces an increase in body weight, which can be reversed with estrogen replacement treatment (Wade et al. 1985). These studies suggest that estrogen plays an important role in the post-menopausal development of obesity.The paraventricular nucleus (PVN) within the hypothalamus is a major center of corticotropin-releasing hormone (CRH) neurons (Sawchenko and Swanson 1985). Previous research has demonstrated that estrogen receptors (ERs) and CRH neurons are co-localized within the PVN (Dagnault and Abbreviations used: a-hCRH, a-helical CRH; CRH, corticotropinreleasing hormone; DMSO, dimethylsulfoxide; DPN, 2,3-bis(4-hydroxyphenyl)-propionitrile; ER, estrogen receptor; FMH, a-fluoromethyl histidine; H1KO, histamine receptors knockout; H1-R, histamine receptors; HDC, histidine decarboxylase; i3vt, intra-3rd ventricular; OVX, ovariectomy; PBS, phosphate-buffered saline; PPT, 4,4¢,4¢¢-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol; PVN, paraventricular nucleus; SCN, suprachiasmatic nucleus; t-MH, tele-methylhistamine; TMN, tuberomammillary nucleus. AbstractMenopause is one of the triggers that induce obesity. Estradiol (E2), corticotropin-releasing hormone (CRH), and hypothalamic neuronal histamine are anorexigenic substances within the hypothalamus. This study examined the interactions among E2, CRH, and histamine during the regulation of feeding behavior and obesity in rodents. Food intake was measured in rats after the treatment of E2, a-fluoromethyl histidine, a specific suicide inhibitor of histidine decarboxylase that depletes hypothalamic neuronal histamine, or CRH antagonist. We measured food intake and body weight in wild-type mice or mice with targeted disruption of the histamine receptors (H1-R) knockout (H1KO mice). Furthermore, we investigated CRH content and histamine turnover in the hypothalamus after the E2 treatment or ovariectomy (OVX). We used immunohistochemical staining for estrogen receptors (ERs) in the histamine neurons. The E2-induced suppression of feeding was partially attenuated in rats pre-treated with a-fluoromethyl histidine or CRH antagonist and in H1KO mice. E2 treatment increased CRH content and histamine turnover in the hypothalamus. OVX increased food intake and body weight, and decreased CRH content and histamine turnover in the hypothalamus. In addition, E2 replacement reversed the OVX-induced changes in food intake and body weight in wild-type mic...

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“…A probe was inserted and fixed in the epididymal WAT through the incision with the aid of a guide cannula. Details of the surgical procedures have been described elsewhere [4,9].…”

Section: Methodsmentioning

confidence: 99%

“…Rats that were to be used for blood collection underwent surgery under ether anaesthesia for implantation of chronically indwelling silicone catheter in the right external jugular vein with its end at a point just outside of the atrium [9]. Surgical catheterizations were performed 7 days prior to the histidine injections.…”

Section: Surgerymentioning

confidence: 99%