l-Ornithine intake affects sympathetic nerve outflows and reduces body weight and food intake in rats

Konishi, Yuuki; Koosaka, Yasutaka; Maruyama, Ryuutaro; Imanishi, Kazuki; Kasahara, Kazuaki; Matsuda, Ai; Akiduki, Saori; Hishida, Yukihiro; Kurata, Yasutaka; Shibamoto, Toshishige; Satomi, Jun; Tanida, Mamoru

doi:10.1016/j.brainresbull.2014.11.004

Cited by 18 publications

(12 citation statements)

References 12 publications

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“…In each ISH experiment, we used DIG‐ or fluorescein‐labelled sense probes for negative controls and confirmed the absence of nonspecific signals in the ARN. Primary antibodies for POMC, TH and kisspeptin used in the present study have been well characterised elsewhere . All of the immunofluorescent images from these antibodies were in good agreement with previous studies and no nonspecific signals were observed in primary antibody‐omitted controls.…”

Section: Methodssupporting

confidence: 88%

Characterisation of Kiss1r (Gpr54)‐Expressing Neurones in the Arcuate Nucleus of the Female Rat Hypothalamus

Higo

Iijima

Ozawa

2017

J Neuroendocrinology

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Kisspeptin is essential in reproduction and acts by stimulating neurones expressing gonadotrophin-releasing hormone (GnRH). Recent studies suggest that kisspeptin has multiple roles in the modulation of neuronal circuits in systems outside the hypothalamic-pituitary-gonadal axis. Our recent research using in situ hybridisation (ISH) clarified the histological distribution of Kiss1r (Gpr54)-expressing neurones in the rat brain that were presumed to be putative targets of kisspeptin. The arcuate nucleus (ARN) of the hypothalamus is one of the brain regions in which Kiss1r expression in non-GnRH neurones is prominent. However, the characteristics of Kiss1r-expressing neurones in the ARN remain unclear. The present study aimed to determine the neurochemical characteristics of Kiss1r-expressing neurones in the ARN using ISH and immunofluorescence. We revealed that the majority (approximately 63%) of Kiss1r-expressing neurones in the ARN were pro-opiomelanocortin (POMC) neurones, which have an anorexic effect in mammals. Additionally, a few Kiss1r-expressing neurones in the dorsal ARN are tuberoinfundibular dopamine (TIDA) neurones, which control milk production by inhibiting prolactin secretion from the anterior pituitary. TIDA neurones showed a relatively weak Kiss1r ISH signal compared to POMC neurones, as well as low co-expression of Kiss1r (approximately 15%). We also examined the expression of Kiss1r in neuropeptide Y and kisspeptin neurones, which are reported to arise from POMC-expressing progenitor cells during development. However, the vast majority of neuropeptide Y and kisspeptin neurones in the ARN did not express Kiss1r. These results suggest that kisspeptin may directly regulate energy homeostasis and milk production by modulating the activity of POMC and TIDA neurones, respectively. Our results provide an insight into the wide variety of roles that kisspeptin plays in homeostatic and neuroendocrine functions.

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Section: Methodssupporting

confidence: 88%

Characterisation of Kiss1r (Gpr54)‐Expressing Neurones in the Arcuate Nucleus of the Female Rat Hypothalamus

Higo

Iijima

Ozawa

2017

J Neuroendocrinology

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“…Earlier studies demonstrated that vagal pathways innervating the gastrointestinal tract, pancreas, and liver are involved in the control of assimilation, storage, mobilization, conversion, and oxidation of macronutrients [75, 76]. Lactobacillus has been hypothesized to modulate fat metabolism via a vagal-dependent pathway [77] and vagal ablation abolished -ornithine positive effects on lipid metabolism [78]. PPARγ signaling in NG has notably been hypothesized to regulate diet-driven thermogenesis [79].…”

Section: Resultsmentioning

confidence: 99%

Diet-driven microbiota dysbiosis is associated with vagal remodeling and obesity

Sen

Cawthon

Ihde

et al. 2017

Physiology & Behavior

200

152

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Obesity is one of the major health issues in the United States. Consumption of diets rich in energy, notably from fats and sugars (high-fat/high-sugar diet: HF/HSD) is linked to the development of obesity and a popular dietary approach for weight loss is to reduce fat intake. Obesity research traditionally uses low and high fat diets and there has been limited investigation of the potential detrimental effects of a low-fat/high-sugar diet (LF/HSD) on body fat accumulation and health. Therefore, in the present study, we investigated the effects of HF/HSD and LF/HSD on microbiota composition, gut inflammation, gut-brain vagal communication and body fat accumulation. Specifically, we tested the hypothesis that LF/HSD changes the gut microbiota, induces gut inflammation and alters vagal gut-brain communication, associated with increased body fat accumulation. Sprague-Dawley rats were fed an HF/HSD, LF/HSD or control low-fat/low-sugar diet (LF/LSD) for 4 weeks. Body weight, caloric intake, and body composition were monitored daily and fecal samples were collected at baseline, 1, 6 and 27 days after the dietary switch. After four weeks, blood and tissues (gut, brain, liver and nodose ganglia) were sampled. Both HF/HSD and LF/HSD-fed rats displayed significant increases in body weight and body fat compared to LF/LSD-fed rats. 16S rRNA sequencing showed that both HF/HSD and LF/HSD-fed animals exhibited gut microbiota dysbiosis characterized by an overall decrease in bacterial diversity and an increase in Firmicutes/Bacteriodetes ratio. Dysbiosis was typified by a bloom in Clostridia and Bacilli and a marked decrease in Lactobacillus spp. LF/HSD-fed animals showed a specific increase in Sutterella and Bilophila, both Proteobacteria, abundances of which have been associated with liver damage. Expression of pro-inflammatory cytokines, such as IL-6, IL-1β and TNFα was upregulated in the cecum while levels of tight junction protein occludin were downregulated in both HF/HSD and LF/HSD fed rats. HF/HSD and LF/HSD-fed rats also exhibited an increase in cecum and serum levels of lipopolysaccharide (LPS), a pro-inflammatory bacterial product. Immunofluorescence revealed the withdrawal of vagal afferents from the gut and at their site of termination the nucleus of the solitary tract (NTS) in both the HF/HSD and LF/HSD rats. Moreover, there was significant microglia activation in the nodose ganglia, which contain the vagal afferent neuron cell bodies, of HF/HSD and LF/HSD rats. Taken together, these data indicate that, similar to HF/HSD, consumption of an LF/HSD induces dysbiosis of gut microbiota, increases gut inflammation and alters vagal gut-brain communication. These changes are associated with an increase in body fat accumulation.

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“…l ‐arginine supplementation increases cAMP production in both BAT and rpWAT and an l ‐arginine‐rich diet increases energy expenditure in rats and reduces energy intake efficiency, general indicators of increased expenditure through mitochondrial uncoupling; however no changes to UCP1 could be detected in WAT or BAT . Alternatively, acute administration of l ‐ornithine, the metabolite of l ‐arginine, increases sympathetic flow to both BAT and eWAT , resulting in increased UCP1 protein expression in BAT (eWAT was not measured).…”

Section: Agents That Increase Browning Of White Adipose Tissuementioning

confidence: 99%

Could burning fat start with a brite spark? Pharmacological and nutritional ways to promote thermogenesis

Merlin

Evans

Dehvari

et al. 2015

Molecular Nutrition Food Res

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There are two types of adipose tissue with distinct functions-white adipose tissue stores chemical energy as triglycerides, whereas brown adipose tissue consumes energy and releases heat (thermogenesis) in response to sympathetic nerve activity. In humans, treatments that promote greater brown adipose tissue deposition and/or activity would be highly beneficial in regimes aimed at reducing obesity. Adult humans have restricted populations of prototypical brown adipocytes in the neck and chest areas, but recent advances have established that adipocytes with similar properties, termed "brite" adipocytes, can be recruited in subcutaneous depots thought to be primarily white adipose tissue. These brite adipocytes express the protein machinery required for thermogenesis, but to assess brite adipocytes as viable therapeutic targets we need to understand how to promote conversion of white adipocytes to brite adipocytes and ways to increase optimal energy consumption and thermogenesis in these brite adipocytes. This can be accomplished by pharmacological and nutritional therapies to differing degrees, as reviewed in detail here.

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l-Ornithine intake affects sympathetic nerve outflows and reduces body weight and food intake in rats

Cited by 18 publications

References 12 publications

Characterisation of Kiss1r (Gpr54)‐Expressing Neurones in the Arcuate Nucleus of the Female Rat Hypothalamus

Characterisation of Kiss1r (Gpr54)‐Expressing Neurones in the Arcuate Nucleus of the Female Rat Hypothalamus

Diet-driven microbiota dysbiosis is associated with vagal remodeling and obesity

Could burning fat start with a brite spark? Pharmacological and nutritional ways to promote thermogenesis

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