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Matured Hop Bittering Components Induce Thermogenesis in Brown Adipose Tissue via Sympathetic Nerve Activity.

Morimoto-Kobayashi Y, Ohara K, Takahashi C, Kitao S, Wang G, Taniguchi Y, Katayama M, Nagai K - PLoS ONE (2015)

Bottom Line: Therefore, we tested MHB for an effect on ameliorating diet-induced body fat accumulation in rodents.MHB ingestion had a beneficial effect but, compared to iso-α-acids and despite containing structurally similar compounds, acted via different mechanisms to reduce body fat accumulation.We also found that uncoupling protein 1 (UCP1) expression in brown adipose tissue (BAT) was significantly increased in MHB-fed mice at both the mRNA and protein levels.

View Article: PubMed Central - PubMed

Affiliation: Research Laboratories for Health Science & Food Technologies, KIRIN Company, Ltd., Yokohama, Kanagawa, Japan.

ABSTRACT
Obesity is the principal symptom of metabolic syndrome, which refers to a group of risk factors that increase the likelihood of atherosclerosis. In recent decades there has been a sharp rise in the incidence of obesity throughout the developed world. Iso-α-acids, the bitter compounds derived from hops in beer, have been shown to prevent diet-induced obesity by increasing lipid oxidation in the liver and inhibition of lipid absorption from the intestine. Whereas the sharp bitterness induced by effective dose of iso-α-acids precludes their acceptance as a nutrient, matured hop bittering components (MHB) appear to be more agreeable. Therefore, we tested MHB for an effect on ameliorating diet-induced body fat accumulation in rodents. MHB ingestion had a beneficial effect but, compared to iso-α-acids and despite containing structurally similar compounds, acted via different mechanisms to reduce body fat accumulation. MHB supplementation significantly reduced body weight gain, epididymal white adipose tissue weight, and plasma non-esterified free fatty acid levels in diet-induced obese mice. We also found that uncoupling protein 1 (UCP1) expression in brown adipose tissue (BAT) was significantly increased in MHB-fed mice at both the mRNA and protein levels. In addition, MHB administration in rats induced the β-adrenergic signaling cascade, which is related to cAMP accumulation in BAT, suggesting that MHB could modulate sympathetic nerve activity innervating BAT (BAT-SNA). Indeed, single oral administration of MHB elevated BAT-SNA in rats, and this elevation was dissipated by subdiaphragmatic vagotomy. Single oral administration of MHB maintained BAT temperature at a significantly higher level than in control rats. Taken together, these findings indicate that MHB ameliorates diet-induced body fat accumulation, at least partly, by enhancing thermogenesis in BAT via BAT-SNA activation. Our data suggests that MHB is a useful tool for developing functional foods or beverages to counteract the accumulation of body fat.

No MeSH data available.


Related in: MedlinePlus

Single oral administration of MHB increased the level of cAMP in BAT and elevated its temperature in rats.(A) cAMP level in the lysates of BAT obtained from rats administered MHB pretreated with propranolol or saline. Thirty minutes after the pretreatment with 10 mg/kg propranolol or saline, rats were administered 10 mg/kg MHB and killed after 3 h. Data are presented as means ± SEM. n = 10 rats/group. **P < 0.01, N.S., not significant (by unpaired Student’s t-test). (B) Time course of BAT temperature changes (ΔTBAT) taken every 1 min relative to the baseline. The baseline was determined as the mean TBAT over a 5-min period before the administration of MHB. Urethane-anesthetized rats were administered 10 mg/kg of MHB. Data are presented as means ± SEM. n = 4 rats/group. **P < 0.01 (by ANOVA with repeated measures).
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pone.0131042.g004: Single oral administration of MHB increased the level of cAMP in BAT and elevated its temperature in rats.(A) cAMP level in the lysates of BAT obtained from rats administered MHB pretreated with propranolol or saline. Thirty minutes after the pretreatment with 10 mg/kg propranolol or saline, rats were administered 10 mg/kg MHB and killed after 3 h. Data are presented as means ± SEM. n = 10 rats/group. **P < 0.01, N.S., not significant (by unpaired Student’s t-test). (B) Time course of BAT temperature changes (ΔTBAT) taken every 1 min relative to the baseline. The baseline was determined as the mean TBAT over a 5-min period before the administration of MHB. Urethane-anesthetized rats were administered 10 mg/kg of MHB. Data are presented as means ± SEM. n = 4 rats/group. **P < 0.01 (by ANOVA with repeated measures).

Mentions: In general, norepinephrine, which is secreted from the sympathetic nerve endings, induces cAMP accumulation via the β3-adrenergic signaling cascade in BAT [4,24]. To confirm the involvement of this mechanism, we measured the cAMP level in BAT 3 h after MHB administration at a dose of 10 mg/kg with or without pretreatment of β-adrenergic antagonist propranolol in rats. MHB induced an increase in the cAMP level (1.9-fold, P < 0.01), while pretreatment with propranolol completely suppressed cAMP induction by MHB (Fig 4A). To confirm whether elevation of BAT-SNA by MHB promotes thermogenesis in BAT, we measured the temperature of BAT (TBAT) in rats using a temperature transmitter. Single oral administration of MHB (10 mg/kg) significantly elevated TBAT compared to that in the control group as shown in Fig 4B (P < 0.01). There was no significant statistical difference between the initial values of the two groups (Mann-Whitney U test).


Matured Hop Bittering Components Induce Thermogenesis in Brown Adipose Tissue via Sympathetic Nerve Activity.

Morimoto-Kobayashi Y, Ohara K, Takahashi C, Kitao S, Wang G, Taniguchi Y, Katayama M, Nagai K - PLoS ONE (2015)

Single oral administration of MHB increased the level of cAMP in BAT and elevated its temperature in rats.(A) cAMP level in the lysates of BAT obtained from rats administered MHB pretreated with propranolol or saline. Thirty minutes after the pretreatment with 10 mg/kg propranolol or saline, rats were administered 10 mg/kg MHB and killed after 3 h. Data are presented as means ± SEM. n = 10 rats/group. **P < 0.01, N.S., not significant (by unpaired Student’s t-test). (B) Time course of BAT temperature changes (ΔTBAT) taken every 1 min relative to the baseline. The baseline was determined as the mean TBAT over a 5-min period before the administration of MHB. Urethane-anesthetized rats were administered 10 mg/kg of MHB. Data are presented as means ± SEM. n = 4 rats/group. **P < 0.01 (by ANOVA with repeated measures).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4476742&req=5

pone.0131042.g004: Single oral administration of MHB increased the level of cAMP in BAT and elevated its temperature in rats.(A) cAMP level in the lysates of BAT obtained from rats administered MHB pretreated with propranolol or saline. Thirty minutes after the pretreatment with 10 mg/kg propranolol or saline, rats were administered 10 mg/kg MHB and killed after 3 h. Data are presented as means ± SEM. n = 10 rats/group. **P < 0.01, N.S., not significant (by unpaired Student’s t-test). (B) Time course of BAT temperature changes (ΔTBAT) taken every 1 min relative to the baseline. The baseline was determined as the mean TBAT over a 5-min period before the administration of MHB. Urethane-anesthetized rats were administered 10 mg/kg of MHB. Data are presented as means ± SEM. n = 4 rats/group. **P < 0.01 (by ANOVA with repeated measures).
Mentions: In general, norepinephrine, which is secreted from the sympathetic nerve endings, induces cAMP accumulation via the β3-adrenergic signaling cascade in BAT [4,24]. To confirm the involvement of this mechanism, we measured the cAMP level in BAT 3 h after MHB administration at a dose of 10 mg/kg with or without pretreatment of β-adrenergic antagonist propranolol in rats. MHB induced an increase in the cAMP level (1.9-fold, P < 0.01), while pretreatment with propranolol completely suppressed cAMP induction by MHB (Fig 4A). To confirm whether elevation of BAT-SNA by MHB promotes thermogenesis in BAT, we measured the temperature of BAT (TBAT) in rats using a temperature transmitter. Single oral administration of MHB (10 mg/kg) significantly elevated TBAT compared to that in the control group as shown in Fig 4B (P < 0.01). There was no significant statistical difference between the initial values of the two groups (Mann-Whitney U test).

Bottom Line: Therefore, we tested MHB for an effect on ameliorating diet-induced body fat accumulation in rodents.MHB ingestion had a beneficial effect but, compared to iso-α-acids and despite containing structurally similar compounds, acted via different mechanisms to reduce body fat accumulation.We also found that uncoupling protein 1 (UCP1) expression in brown adipose tissue (BAT) was significantly increased in MHB-fed mice at both the mRNA and protein levels.

View Article: PubMed Central - PubMed

Affiliation: Research Laboratories for Health Science & Food Technologies, KIRIN Company, Ltd., Yokohama, Kanagawa, Japan.

ABSTRACT
Obesity is the principal symptom of metabolic syndrome, which refers to a group of risk factors that increase the likelihood of atherosclerosis. In recent decades there has been a sharp rise in the incidence of obesity throughout the developed world. Iso-α-acids, the bitter compounds derived from hops in beer, have been shown to prevent diet-induced obesity by increasing lipid oxidation in the liver and inhibition of lipid absorption from the intestine. Whereas the sharp bitterness induced by effective dose of iso-α-acids precludes their acceptance as a nutrient, matured hop bittering components (MHB) appear to be more agreeable. Therefore, we tested MHB for an effect on ameliorating diet-induced body fat accumulation in rodents. MHB ingestion had a beneficial effect but, compared to iso-α-acids and despite containing structurally similar compounds, acted via different mechanisms to reduce body fat accumulation. MHB supplementation significantly reduced body weight gain, epididymal white adipose tissue weight, and plasma non-esterified free fatty acid levels in diet-induced obese mice. We also found that uncoupling protein 1 (UCP1) expression in brown adipose tissue (BAT) was significantly increased in MHB-fed mice at both the mRNA and protein levels. In addition, MHB administration in rats induced the β-adrenergic signaling cascade, which is related to cAMP accumulation in BAT, suggesting that MHB could modulate sympathetic nerve activity innervating BAT (BAT-SNA). Indeed, single oral administration of MHB elevated BAT-SNA in rats, and this elevation was dissipated by subdiaphragmatic vagotomy. Single oral administration of MHB maintained BAT temperature at a significantly higher level than in control rats. Taken together, these findings indicate that MHB ameliorates diet-induced body fat accumulation, at least partly, by enhancing thermogenesis in BAT via BAT-SNA activation. Our data suggests that MHB is a useful tool for developing functional foods or beverages to counteract the accumulation of body fat.

No MeSH data available.


Related in: MedlinePlus