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Olfactory stimulation with scent of grapefruit oil affects autonomic nerves, lipolysis and appetite in rats.
Shen J, Niijima A, Tanida M, Horii Y, Maeda K, Nagai K.
Division of Protein Metabolism, Institute for Protein Research, Osaka University, 3-2 Yamada-Oka, Suita, Osaka 565-0871, Japan.
In a previous study, we found that olfactory stimulation with scent of grapefruit oil (SGFO) excites the sympathetic nerve innervating the white adipose tissue in rats. Here we further examined the effects of SGFO in rats and observed that olfactory stimulation with SGFO excited the sympathetic nerves innervating the brown adipose tissue and adrenal gland and inhibited the parasympathetic gastric nerve. Local anesthesia of the nasal mucosa with xylocaine or anosmic treatment using ZnSO(4) eliminated the autonomic changes caused by SGFO. Moreover, stimulation with SGFO elevated the plasma glycerol level, and treatment with either ZnSO(4) or an intraperitoneal injection of diphenhydramine, a histamine H1 receptor-antagonist, abolished the glycerol elevation by SGFO. Furthermore, a 15-min exposure to SGFO three times a week reduced food intake and body weight. Finally, limonene, a component of grapefruit oil, induced reponses similar to those caused by SGFO, and diphenhydramine eliminated the glycerol response to limonene. Thus, the scent of grapefruit oil, and particularly its primary component limonene, affects autonomic nerves, enhances lipolysis through a histaminergic response, and reduces appetite and body weight.
PMID: 15862904 [PubMed - in process]
Anti-obese action of raspberry ketone.
Morimoto C, Satoh Y, Hara M, Inoue S, Tsujita T, Okuda H.
Department of Medical Biochemistry, Ehime University School of Medicine, Shigenobu-cho, Onsen-gun, Ehime 791-0295, Japan.
Raspberry ketone (4-(4-hydroxyphenyl) butan-2-one; RK) is a major aromatic compound of red raspberry (Rubus idaeus). The structure of RK is similar to the structures of capsaicin and synephrine, compounds known to exert anti-obese actions and alter the lipid metabolism. The present study was performed to clarify whether RK helps prevent obesity and activate lipid metabolism in rodents. To test the effect on obesity, our group designed the following in vivo experiments: 1) mice were fed a high-fat diet including 0.5, 1, or 2% of RK for 10 weeks; 2) mice were given a high-fat diet for 6 weeks and subsequently fed the same high-fat diet containing1% RK for the next 5 weeks. RK prevented the high-fat-diet-induced elevations in body weight and the weights of the liver and visceral adipose tissues (epididymal, retroperitoneal, and mesenteric). RK also decreased these weights and hepatic triacylglycerol content after they had been increased by a high-fat diet. RK significantly increased norepinephrine-induced lipolysis associated with the translocation of hormone-sensitive lipase from the cytosol to lipid droplets in rat epididymal fat cells. In conclusion, RK prevents and improves obesity and fatty liver. These effects appear to stem from the action of RK in altering the lipid metabolism, or more specifically, in increasing norepinephrine-induced lipolysis in white adipocytes.
PMID: 15862604 [PubMed - in process]
Ingested cocoa can prevent high-fat diet-induced obesity by regulating the expression of genes for fatty acid metabolism.
Matsui N, Ito R, Nishimura E, Yoshikawa M, Kato M, Kamei M, Shibata H, Matsumoto I, Abe K, Hashizume S.
Research Institute, Morinaga & Co., Ltd., Kanagawa, Japan.
OBJECTIVE: We previously found that ingested cocoa decreased visceral adipose tissue weight in rat. To elucidate the molecular mechanisms of that effect, we carried out experiments aimed at analyzing biochemical parameters and gene expression profiles. METHODS: Rats were fed either of two high-fat diets, differing only in supplementation with real or mimetic cocoa. On day 21, body weights, mesenteric white adipose tissue weights, and concentrations of serum triacylglycerol were measured. To investigate the molecular mechanisms underlying the effects of cocoa on lipid metabolism and triacylglycerol accumulation, we examined gene expression profiles in liver and mesenteric white adipose tissues using the GeneChip microarray system. RESULTS: Final body weights and mesenteric white adipose tissue weights were significantly lower in rats fed the real cocoa diet than in those fed the mimetic cocoa diet (P < 0.05), and serum triacylglycerol concentrations tended to be lower in rats fed the real cocoa diet (P = 0.072). DNA microarray analysis showed that cocoa ingestion suppressed the expression of genes for enzymes involved in fatty acid synthesis in liver and white adipose tissues. In white adipose tissue, cocoa ingestion also decreased the expression of genes for fatty acid transport-relating molecules, whereas it upregulated the expression of genes for uncoupling protein-2 as a thermogenesis factor. CONCLUSIONS: Ingested cocoa can prevent high-fat diet-induced obesity by modulating lipid metabolism, especially by decreasing fatty acid synthesis and transport systems, and enhancement of part of the thermogenesis mechanism in liver and white adipose tissue.
PMID: 15850966 [PubMed - in process]
Dietary L-arginine supplementation reduces fat mass in Zucker diabetic fatty rats.
Fu WJ, Haynes TE, Kohli R, Hu J, Shi W, Spencer TE, Carroll RJ, Meininger CJ, Wu G.
Faculty of Nutrition, Texas A&M University, College Station, TX 77843, USA.
This study was conducted to test the hypothesis that dietary supplementation of arginine, the physiologic precursor of nitric oxide (NO), reduces fat mass in the Zucker diabetic fatty (ZDF) rat, a genetically obese animal model of type-II diabetes mellitus. Male ZDF rats, 9 wk old, were pair-fed Purina 5008 diet and received drinking water containing arginine-HCl (1.51%) or alanine (2.55%, isonitrogenous control) for 10 wk. Serum concentrations of arginine and NO(x) (oxidation products of NO) were 261 and 70% higher, respectively, in arginine-supplemented rats than in control rats. The body weights of arginine-treated rats were 6, 10, and 16% lower at wk 4, 7, and 10 after the treatment initiation, respectively, compared with control rats. Arginine supplementation reduced the weight of abdominal (retroperitoneal) and epididymal adipose tissues (45 and 25%, respectively) as well as serum concentrations of glucose (25%), triglycerides (23%), FFA (27%), homocysteine (26%), dimethylarginines (18-21%), and leptin (32%). The arginine treatment enhanced NO production (71-85%), lipolysis (22-24%), and the oxidation of glucose (34-36%) and octanoate (40-43%) in abdominal and epididymal adipose tissues. Results of the microarray analysis indicated that arginine supplementation increased adipose tissue expression of key genes responsible for fatty acid and glucose oxidation: NO synthase-1 (145%), heme oxygenase-3 (789%), AMP-activated protein kinase (123%), and peroxisome proliferator-activated receptor gamma coactivator-1alpha (500%). The induction of these genes was verified by real-time RT-PCR analysis. In sum, arginine treatment may provide a potentially novel and useful means to enhance NO synthesis and reduce fat mass in obese subjects with type-II diabetes mellitus.
PMID: 15795423 [PubMed - in process]
Shen J, Niijima A, Tanida M, Horii Y, Maeda K, Nagai K.
Division of Protein Metabolism, Institute for Protein Research, Osaka University, 3-2 Yamada-Oka, Suita, Osaka 565-0871, Japan.
In a previous study, we found that olfactory stimulation with scent of grapefruit oil (SGFO) excites the sympathetic nerve innervating the white adipose tissue in rats. Here we further examined the effects of SGFO in rats and observed that olfactory stimulation with SGFO excited the sympathetic nerves innervating the brown adipose tissue and adrenal gland and inhibited the parasympathetic gastric nerve. Local anesthesia of the nasal mucosa with xylocaine or anosmic treatment using ZnSO(4) eliminated the autonomic changes caused by SGFO. Moreover, stimulation with SGFO elevated the plasma glycerol level, and treatment with either ZnSO(4) or an intraperitoneal injection of diphenhydramine, a histamine H1 receptor-antagonist, abolished the glycerol elevation by SGFO. Furthermore, a 15-min exposure to SGFO three times a week reduced food intake and body weight. Finally, limonene, a component of grapefruit oil, induced reponses similar to those caused by SGFO, and diphenhydramine eliminated the glycerol response to limonene. Thus, the scent of grapefruit oil, and particularly its primary component limonene, affects autonomic nerves, enhances lipolysis through a histaminergic response, and reduces appetite and body weight.
PMID: 15862904 [PubMed - in process]
Anti-obese action of raspberry ketone.
Morimoto C, Satoh Y, Hara M, Inoue S, Tsujita T, Okuda H.
Department of Medical Biochemistry, Ehime University School of Medicine, Shigenobu-cho, Onsen-gun, Ehime 791-0295, Japan.
Raspberry ketone (4-(4-hydroxyphenyl) butan-2-one; RK) is a major aromatic compound of red raspberry (Rubus idaeus). The structure of RK is similar to the structures of capsaicin and synephrine, compounds known to exert anti-obese actions and alter the lipid metabolism. The present study was performed to clarify whether RK helps prevent obesity and activate lipid metabolism in rodents. To test the effect on obesity, our group designed the following in vivo experiments: 1) mice were fed a high-fat diet including 0.5, 1, or 2% of RK for 10 weeks; 2) mice were given a high-fat diet for 6 weeks and subsequently fed the same high-fat diet containing1% RK for the next 5 weeks. RK prevented the high-fat-diet-induced elevations in body weight and the weights of the liver and visceral adipose tissues (epididymal, retroperitoneal, and mesenteric). RK also decreased these weights and hepatic triacylglycerol content after they had been increased by a high-fat diet. RK significantly increased norepinephrine-induced lipolysis associated with the translocation of hormone-sensitive lipase from the cytosol to lipid droplets in rat epididymal fat cells. In conclusion, RK prevents and improves obesity and fatty liver. These effects appear to stem from the action of RK in altering the lipid metabolism, or more specifically, in increasing norepinephrine-induced lipolysis in white adipocytes.
PMID: 15862604 [PubMed - in process]
Ingested cocoa can prevent high-fat diet-induced obesity by regulating the expression of genes for fatty acid metabolism.
Matsui N, Ito R, Nishimura E, Yoshikawa M, Kato M, Kamei M, Shibata H, Matsumoto I, Abe K, Hashizume S.
Research Institute, Morinaga & Co., Ltd., Kanagawa, Japan.
OBJECTIVE: We previously found that ingested cocoa decreased visceral adipose tissue weight in rat. To elucidate the molecular mechanisms of that effect, we carried out experiments aimed at analyzing biochemical parameters and gene expression profiles. METHODS: Rats were fed either of two high-fat diets, differing only in supplementation with real or mimetic cocoa. On day 21, body weights, mesenteric white adipose tissue weights, and concentrations of serum triacylglycerol were measured. To investigate the molecular mechanisms underlying the effects of cocoa on lipid metabolism and triacylglycerol accumulation, we examined gene expression profiles in liver and mesenteric white adipose tissues using the GeneChip microarray system. RESULTS: Final body weights and mesenteric white adipose tissue weights were significantly lower in rats fed the real cocoa diet than in those fed the mimetic cocoa diet (P < 0.05), and serum triacylglycerol concentrations tended to be lower in rats fed the real cocoa diet (P = 0.072). DNA microarray analysis showed that cocoa ingestion suppressed the expression of genes for enzymes involved in fatty acid synthesis in liver and white adipose tissues. In white adipose tissue, cocoa ingestion also decreased the expression of genes for fatty acid transport-relating molecules, whereas it upregulated the expression of genes for uncoupling protein-2 as a thermogenesis factor. CONCLUSIONS: Ingested cocoa can prevent high-fat diet-induced obesity by modulating lipid metabolism, especially by decreasing fatty acid synthesis and transport systems, and enhancement of part of the thermogenesis mechanism in liver and white adipose tissue.
PMID: 15850966 [PubMed - in process]
Dietary L-arginine supplementation reduces fat mass in Zucker diabetic fatty rats.
Fu WJ, Haynes TE, Kohli R, Hu J, Shi W, Spencer TE, Carroll RJ, Meininger CJ, Wu G.
Faculty of Nutrition, Texas A&M University, College Station, TX 77843, USA.
This study was conducted to test the hypothesis that dietary supplementation of arginine, the physiologic precursor of nitric oxide (NO), reduces fat mass in the Zucker diabetic fatty (ZDF) rat, a genetically obese animal model of type-II diabetes mellitus. Male ZDF rats, 9 wk old, were pair-fed Purina 5008 diet and received drinking water containing arginine-HCl (1.51%) or alanine (2.55%, isonitrogenous control) for 10 wk. Serum concentrations of arginine and NO(x) (oxidation products of NO) were 261 and 70% higher, respectively, in arginine-supplemented rats than in control rats. The body weights of arginine-treated rats were 6, 10, and 16% lower at wk 4, 7, and 10 after the treatment initiation, respectively, compared with control rats. Arginine supplementation reduced the weight of abdominal (retroperitoneal) and epididymal adipose tissues (45 and 25%, respectively) as well as serum concentrations of glucose (25%), triglycerides (23%), FFA (27%), homocysteine (26%), dimethylarginines (18-21%), and leptin (32%). The arginine treatment enhanced NO production (71-85%), lipolysis (22-24%), and the oxidation of glucose (34-36%) and octanoate (40-43%) in abdominal and epididymal adipose tissues. Results of the microarray analysis indicated that arginine supplementation increased adipose tissue expression of key genes responsible for fatty acid and glucose oxidation: NO synthase-1 (145%), heme oxygenase-3 (789%), AMP-activated protein kinase (123%), and peroxisome proliferator-activated receptor gamma coactivator-1alpha (500%). The induction of these genes was verified by real-time RT-PCR analysis. In sum, arginine treatment may provide a potentially novel and useful means to enhance NO synthesis and reduce fat mass in obese subjects with type-II diabetes mellitus.
PMID: 15795423 [PubMed - in process]
