Comparison of the sympathetic stimulatory abilities of B-type procyanidins based on induction of uncoupling protein-1 in brown adipose tissue (BAT) and increased plasma catecholamine (CA) in mice
Abstract:ObjectivesWe previously found that elevated energy expenditure following a single oral dose of flavan 3-ols (FL), a mixture of catechins and B type procyanidins, is caused by sympathetic nerve activation. In the present study, we compared the activity of the FL components (-)-epicatechin (EC; monomer), procyanidin B2 (B2; dimer), procyanidin C1 (C1; trimer), cinnamtannin A2 (A2; tetramer), and more than pentamer fraction (P5).MethodsMale ICR mice were treated with a single oral dose of FL, EC, B2, C1, A2, or P… Show more
“…Flavonoids may promote brown preadipocyte differentiation, inhibit apoptosis and produce inflammatory factors in BAT. Flavonoids elevate energy expenditure by activating the sympathetic nervous system and increasing UCP-1 mRNA in BAT and plasma catecholamine [124]. Fig.…”
Background
Flavonoids are a class of plant and fungus secondary metabolites and are the most common group of polyphenolic compounds in the human diet. In recent studies, flavonoids have been shown to induce browning of white adipocytes, increase energy consumption, inhibit high-fat diet (HFD)-induced obesity and improve metabolic status. Promoting the activity of brown adipose tissue (BAT) and inducing white adipose tissue (WAT) browning are promising means to increase energy expenditure and improve glucose and lipid metabolism. This review summarizes recent advances in the knowledge of flavonoid compounds and their metabolites.
Methods
We searched the following databases for all research related to flavonoids and WAT browning published through March 2019: PubMed, MEDLINE, EMBASE, and the Web of Science. All included studies are summarized and listed in Table
1
.
Result
We summarized the effects of flavonoids on fat metabolism and the specific underlying mechanisms in sub-categories. Flavonoids activated the sympathetic nervous system (SNS), promoted the release of adrenaline and thyroid hormones to increase thermogenesis and induced WAT browning through the AMPK-PGC-1α/Sirt1 and PPAR signalling pathways. Flavonoids may also promote brown preadipocyte differentiation, inhibit apoptosis and produce inflammatory factors in BAT.
Conclusion
Flavonoids induced WAT browning and activated BAT to increase energy consumption and non-shivering thermogenesis, thus inhibiting weight gain and preventing metabolic diseases.
“…Flavonoids may promote brown preadipocyte differentiation, inhibit apoptosis and produce inflammatory factors in BAT. Flavonoids elevate energy expenditure by activating the sympathetic nervous system and increasing UCP-1 mRNA in BAT and plasma catecholamine [124]. Fig.…”
Background
Flavonoids are a class of plant and fungus secondary metabolites and are the most common group of polyphenolic compounds in the human diet. In recent studies, flavonoids have been shown to induce browning of white adipocytes, increase energy consumption, inhibit high-fat diet (HFD)-induced obesity and improve metabolic status. Promoting the activity of brown adipose tissue (BAT) and inducing white adipose tissue (WAT) browning are promising means to increase energy expenditure and improve glucose and lipid metabolism. This review summarizes recent advances in the knowledge of flavonoid compounds and their metabolites.
Methods
We searched the following databases for all research related to flavonoids and WAT browning published through March 2019: PubMed, MEDLINE, EMBASE, and the Web of Science. All included studies are summarized and listed in Table
1
.
Result
We summarized the effects of flavonoids on fat metabolism and the specific underlying mechanisms in sub-categories. Flavonoids activated the sympathetic nervous system (SNS), promoted the release of adrenaline and thyroid hormones to increase thermogenesis and induced WAT browning through the AMPK-PGC-1α/Sirt1 and PPAR signalling pathways. Flavonoids may also promote brown preadipocyte differentiation, inhibit apoptosis and produce inflammatory factors in BAT.
Conclusion
Flavonoids induced WAT browning and activated BAT to increase energy consumption and non-shivering thermogenesis, thus inhibiting weight gain and preventing metabolic diseases.
“…The capacity of flavanols on activating BAT has been described even with a single dose of a flavanol mixture that included catechins and B type procyanidins or by administering individual components by itself [ 182 ]. In these animals, Ucp1 mRNA expression in BAT and levels of catecholamines in plasma were significantly increased via SNS stimulation but with varying efficacy depending on the stereochemical structure of flavanols [ 182 ]. It should be noted that prolonged ingestion of a catechin-rich beverage increased the BAT density with a decrease in extramyocellular lipids in humans [ 183 ].…”
The prevention and treatment of obesity is primary based on the follow-up of a healthy lifestyle, which includes a healthy diet with an important presence of bioactive compounds such as polyphenols. For many years, the health benefits of polyphenols have been attributed to their anti-oxidant capacity as free radical scavengers. More recently it has been described that polyphenols activate other cell-signaling pathways that are not related to ROS production but rather involved in metabolic regulation. In this review, we have summarized the current knowledge in this field by focusing on the metabolic effects of flavonoids. Flavonoids are widely distributed in the plant kingdom where they are used for growing and defensing. They are structurally characterized by two benzene rings and a heterocyclic pyrone ring and based on the oxidation and saturation status of the heterocyclic ring flavonoids are grouped in seven different subclasses. The present work is focused on describing the molecular mechanisms underlying the metabolic impact of flavonoids in obesity and obesity-related diseases. We described the effects of each group of flavonoids in liver, white and brown adipose tissue and central nervous system and the metabolic and signaling pathways involved on them.
“…In addition, A2 had potent metabolic activity compared with the other procyanidins. (19)(20)(21) In conclusion, stress response induction mechanisms by A2 remains unknown. Further experiments are needed to clarify this, especially, it is needed to elucidate a target molecule in the gastrointestinal tract that recognizes A2, since A2 suggested to have a particular affinity for it.…”
Section: Discussionmentioning
confidence: 94%
“…(19,20) A single oral administration of 1 mg/kg A2 significantly elevated uncoupling protein-1 mRNA in brown adipose tissue; while, procyanidin B2 (dimer) or procyanidin C1 (trimer) showed similar activity at a high dose of 1,000 mg/kg. (21) In addition, a high dose of A2 (100 mg/kg) did not lead to UCP-1 upregulation alone, it only did when combined with an a2 adrenaline blocker. Since the a2 adrenergic receptor, an inhibitory receptor, is present mainly in the central nervous system, those results suggested that a single oral dose of A2 affected the central nervous system and consequently elevated sympathetic nerve activity.…”
Cinnamtannin A2, an (−) epicatechin tetramer, was reported to have potent physiological activity. Cinnamtannin A2 is rarely absorbed from the gastrointestinal tract into the blood and the mechanisms of its beneficial activities are unknown. Cinnamtannin A2 reported to increase sympathetic nervous activity, which was induced by various stressors. In present study, we examined the stress response in the mouse paraventricular nucleus following a single oral dose of cinnamtannin A2 by monitoring mRNA expres sion of corticotropin releasing hormone (CRH) and c fos using in situ hybridization. Corticotropin releasing hormone mRNA showed a tendency to increase at 15 min and significantly increased at 60 min following a single oral administration of 100 µg/kg cinnamtannin A2. After a single dose of 10 µg/kg cinnamtannin A2, there was significant upregulation of CRH mRNA at 60 min. These results suggested that cinnamtannin A2 was recognized as a stressor in central nervous system and this may lead to its beneficial effects on circulation and metabolism.
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