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Functional Foods: Regulation of Metabolism from Molecule to System and Disease Control

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A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 53895

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Special Issue Editor

Prof. Dr. Toshihiko Yada

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Guest Editor

1. Department of Diabetes, Endocrinology and Metabolism, Gifu University Graduate School of Medicine, 2N12(2N18), Yanagido 1-1, Gifu 501-1194, Japan
2. Center for Integrative Physiology, Kansai Electric Power Medical Research Institute, Nakagyo-ku, Kyoto 604-8436, Japan
Interests: feeding center; gut hormone; obesity; anorexia; frailty; rare sugar; Japanese kampo medicine; diet; diabetes
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Special Issue Information

Dear Colleagues,

The obesity is a serious worldwide health problem. Obesity is a major risk factor for type 2 diabetes, cardiovascular diseases, and several kinds of cancer. In addition, in modern societies, subjects with sarcopenia and/or frailty are rapidly increasing. However, few effective and safe medicines are available to treat obesity, sarcopenia and/or frailty. Since these are the lifestyle-related diseases and diet is the most influential part of lifestyle, intervention of these diseases by foods is a promising way.

Obesity is caused by the imbalance of energy intake (feeding) and expenditure as well as disrupted diurnal rhythm. Sarcopenia and frailty involve various peripheral and central symptoms, and underneath abnormal metabolism and feeding behavior play key roles. In this Special Issue, we welcome manuscripts that aim to clarify dysregulated metabolism and feeding behavior in obesity, sarcopenia, frailty and related diseases, and to explore functional foods including herbal medicines to normalize the metabolism and feeding behavior and eventually prevent/treat these diseases. The studies elucidating the underlying action mechanisms from molecular to system are highly encouraged. This includes original research and reviews.

Prof. Dr. Toshihiko Yada
Guest Editor

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

functional food
herbal medicine
metabolism
feeding
obesity
frailty
sarcopenia
diurnal rhythm
gut–brain coupling

Published Papers (14 papers)

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Research

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15 pages, 2359 KiB

Open AccessArticle

Effect of 4-Week Consumption of Soy Kori-tofu on Cardiometabolic Health Markers: A Double-Blind Randomized Controlled Cross-Over Trial in Adults with Mildly Elevated Cholesterol Levels

by Maartje van den Belt, Sandra van der Haar, Els Oosterink, Tom van Loenhout, Takahiro Ishiguro and Diederik Esser

Nutrients 2023, 15(1), 49; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15010049 - 22 Dec 2022

Viewed by 2453

Abstract

Kori-tofu is a frozen soy tofu, and soy consumption is associated with positive effects on cardiometabolic health markers. We aimed to assess the potential of Kori-tofu to improve cardiometabolic health outcomes in humans by repetitive daily consumption. In a double-blind randomized controlled cross-over trial, 45 subjects aged 40–70 years with (mildly) elevated cholesterol levels, received a four week Kori-tofu intervention or whey protein control intervention with a four week wash-out period in between. Cardiometabolic biomarkers were measured before and after both interventions. A significant decrease in total, low-density lipids (LDL), and high-density lipids (HDL) cholesterol, Hemoglobin A1c (HbA1c), fructosamine and systolic blood pressure was observed within the Kori-tofu intervention. However, many of these findings were also observed in the control intervention. Only adiponectin changes were different between treatments but did not change significantly within interventions. Improvements in cardiometabolic markers within the Kori-tofu intervention point toward potential beneficial health effects. Due to the lack of significant effects as compared to control, there is, however, currently no substantiating evidence to claim that Kori-tofu has beneficial effects on cardiometabolic health. Full article

(This article belongs to the Special Issue Functional Foods: Regulation of Metabolism from Molecule to System and Disease Control)

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12 pages, 2415 KiB

Open AccessArticle

Suppressive Effects of Turmeric Extract on Muscle Atrophy in Dexamethasone-Treated Mice and Myotubes

by Kyohei Furukawa, Marika Kousaka, Huijuan Jia and Hisanori Kato

Nutrients 2022, 14(19), 3979; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14193979 - 25 Sep 2022

Cited by 1 | Viewed by 2364

Abstract

Sarcopenia is the decline in skeletal muscle mass, strength, and functions, which decreases the quality of life in elderly people. This study investigated the suppressive effect of turmeric (Curcuma longa) extract (TE) on muscle atrophy in dexamethasone (DEX)-treated mice and C2C12 myotubes. DEX treatment significantly decreased the muscle weight and significantly increased Fbxo32 and Murf1 expression in mice, and these changes were suppressed by the supplementation of an AIN-93 based diet with 2% TE. A similar pattern was observed in FBXO32 and MuRF1 protein expression. In C2C12 myotubes, DEX treatment significantly increased FBXO32 and MuRF1 gene and protein expression, and these increases were significantly suppressed by TE supplementation at a concentration of 200 µg/mL. Furthermore, one of the five TE fractions, which were separated by high-performance liquid chromatography had a similar effect with TE supplementation. The present study proposes the suppressive effect of turmeric on sarcopenia. Full article

(This article belongs to the Special Issue Functional Foods: Regulation of Metabolism from Molecule to System and Disease Control)

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12 pages, 1075 KiB

Open AccessArticle

d-Allulose Inhibits Ghrelin-Responsive, Glucose-Sensitive and Neuropeptide Y Neurons in the Arcuate Nucleus and Central Injection Suppresses Appetite-Associated Food Intake in Mice

by Yermek Rakhat, Kentaro Kaneko, Lei Wang, Wanxin Han, Yutaka Seino, Daisuke Yabe and Toshihiko Yada

Nutrients 2022, 14(15), 3117; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14153117 - 29 Jul 2022

Cited by 2 | Viewed by 2408

Abstract

d-allulose, a rare sugar, has sweetness with few calories. d-allulose regulates feeding and glycemia, and ameliorates hyperphagia, obesity and diabetes. All these functions involve the central nervous system. However, central mechanisms underlying these effects of d-allulose remain unknown. We recently reported that d-allulose activates the anorexigenic neurons in the hypothalamic arcuate nucleus (ARC), the neurons that respond to glucagon-like peptide-1 and that express proopiomelanocortin. However, its action on the orexigenic neurons remains unknown. This study investigated the effects of d-allulose on the ARC neurons implicated in hunger, by measuring cytosolic Ca²⁺ concentration ([Ca²⁺]_i) in single neurons. d-allulose depressed the increases in [Ca²⁺]_i induced by ghrelin and by low glucose in ARC neurons and inhibited spontaneous oscillatory [Ca²⁺]_i increases in neuropeptide Y (NPY) neurons. d-allulose inhibited 10 of 35 (28%) ghrelin-responsive, 18 of 60 (30%) glucose-sensitive and 3 of 8 (37.5%) NPY neurons in ARC. Intracerebroventricular injection of d-allulose inhibited food intake at 20:00 and 22:00, the early dark phase when hunger is promoted. These results indicate that d-allulose suppresses hunger-associated feeding and inhibits hunger-promoting neurons in ARC. These central actions of d-allulose represent the potential of d-allulose to inhibit the hyperphagia with excessive appetite, thereby counteracting obesity and diabetes. Full article

(This article belongs to the Special Issue Functional Foods: Regulation of Metabolism from Molecule to System and Disease Control)

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12 pages, 2744 KiB

Open AccessArticle

TRPV1-Mediated Sensing of Sodium and Osmotic Pressure in POMC Neurons in the Arcuate Nucleus of the Hypothalamus

by Boyang Zhang, Kazuomi Kario, Toshihiko Yada and Masanori Nakata

Nutrients 2022, 14(13), 2600; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14132600 - 23 Jun 2022

Cited by 2 | Viewed by 2078

Abstract

The central melanocortin system conducted by anorexigenic pro-opiomelanocortin (POMC) neurons and orexigenic agouti-related peptide (AgRP) neurons in the arcuate nucleus of the hypothalamus (ARC) not only regulates feeding behavior but also blood pressure. Excessive salt intake raises the Na⁺ concentration ([Na⁺]) in the cerebrospinal fluid (CSF) and worsens hypertension. The blood–brain barrier is immature in the ARC. Therefore, both AgRP and POMC neurons in the ARC have easy access to the electrolytes in the blood and can sense changes in their concentrations. However, the sensitivity of AgRP and POMC neurons to Na⁺ remains unclear. This study aimed to explore how the changes in the extracellular Na⁺ concentration ([Na⁺]) influence these neurons by measuring the cytosolic Ca²⁺ concentration ([Ca²⁺]_i) in the single neurons isolated from the ARC that were subsequently immunocytochemically identified as AgRP or POMC neurons. Both AgRP and POMC neurons responded to increases in both [Na⁺] and osmolarity in C57BL/6 mice. In contrast, in transient receptor potential vanilloid 1 (TRPV1) knockout (KO) mice, POMC neurons failed to respond to increases in both [Na⁺] and osmolarity, while they responded to high glucose and angiotensin II levels with increases in [Ca²⁺]_i. Moreover, in KO mice fed a high-salt diet, the expression of POMC was lower than that in wild-type mice. These results demonstrate that changes in [Na⁺] and osmolarity are sensed by the ARC POMC neurons via the TRPV1-dependent mechanism. Full article

(This article belongs to the Special Issue Functional Foods: Regulation of Metabolism from Molecule to System and Disease Control)

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18 pages, 6332 KiB

Open AccessArticle

A Short-Term Sucrose Diet Impacts Cell Proliferation of Neural Precursors in the Adult Hypothalamus

by Antonia Recabal, Sergio López, Magdiel Salgado, Alejandra Palma, Ana M. Obregón, Roberto Elizondo-Vega, Juan C. Sáez and María Á. García-Robles

Nutrients 2022, 14(13), 2564; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14132564 - 21 Jun 2022

Viewed by 1984

Abstract

Radial glia-like cells in the hypothalamus and dorsal vagal complex are neural precursors (NPs) located near subventricular organs: median eminence and area postrema, respectively. Their strategic position can detect blood-borne nutrients, hormones, and mitogenic signals. Hypothalamic NPs increase their proliferation with a mechanism that involves hemichannel (HC) activity. NPs can originate new neurons in response to a short-term high-fat diet as a compensatory mechanism. The effects of high carbohydrate Western diets on adult neurogenesis are unknown. Although sugars are usually consumed as sucrose, more free fructose is now incorporated into food items. Here, we studied the proliferation of both types of NPs in Sprague Dawley rats exposed to a short-term high sucrose diet (HSD) and a control diet. In tanycyte cultures, we evaluated the effects of glucose and fructose and a mix of both hexoses on HC activity. In rats fed an HSD, we observed an increase in the proliferative state of both precursors. Glucose, either in the presence or absence of fructose, but not fructose alone, induced in vitro HC activity. These results should broaden the understanding of the nutrient monitoring capacity of NPs in reacting to changes in feeding behavior, specifically to high sugar western diets. Full article

(This article belongs to the Special Issue Functional Foods: Regulation of Metabolism from Molecule to System and Disease Control)

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15 pages, 2015 KiB

Open AccessArticle

Dietary Gamma-Aminobutyric Acid (GABA) Induces Satiation by Enhancing the Postprandial Activation of Vagal Afferent Nerves

by Utano Nakamura, Taichi Nohmi, Riho Sagane, Jun Hai, Kento Ohbayashi, Maiko Miyazaki, Atsushi Yamatsu, Mujo Kim and Yusaku Iwasaki

Nutrients 2022, 14(12), 2492; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14122492 - 16 Jun 2022

Cited by 7 | Viewed by 5342

Abstract

Gamma-aminobutyric acid (GABA) is present in the mammalian brain as the main inhibitory neurotransmitter and in foods. It is widely used as a supplement that regulates brain function through stress-reducing and sleep-enhancing effects. However, its underlying mechanisms remain poorly understood, as it is reportedly unable to cross the blood–brain barrier. Here, we explored whether a single peroral administration of GABA affects feeding behavior as an evaluation of brain function and the involvement of vagal afferent nerves. Peroral GABA at 20 and 200 mg/kg immediately before refeeding suppressed short-term food intake without aversive behaviors in mice. However, GABA administration 30 min before refeeding demonstrated no effects. A rise in circulating GABA concentrations by the peroral administration of 200 mg/kg GABA was similar to that by the intraperitoneal injection of 20 mg/kg GABA, which did not alter feeding. The feeding suppression by peroral GABA was blunted by the denervation of vagal afferents. Unexpectedly, peroral GABA alone did not alter vagal afferent activities histologically. The coadministration of a liquid diet and GABA potentiated the postprandial activation of vagal afferents, thereby enhancing postprandial satiation. In conclusion, dietary GABA activates vagal afferents in collaboration with meals or meal-evoked factors and regulates brain function including feeding behavior. Full article

(This article belongs to the Special Issue Functional Foods: Regulation of Metabolism from Molecule to System and Disease Control)

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11 pages, 2679 KiB

Open AccessArticle

New Mechanisms of Bromelain in Alleviating Non-Alcoholic Fatty Liver Disease-Induced Deregulation of Blood Coagulation

by Po-An Hu, Sz-Han Wang, Chia-Hui Chen, Bei-Chia Guo, Jenq-Wen Huang and Tzong-Shyuan Lee

Nutrients 2022, 14(11), 2329; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14112329 - 01 Jun 2022

Cited by 2 | Viewed by 3610

Abstract

Bromelain, an enzyme extracted from the stems of pineapples, exerts anticoagulant effects; however, the regulatory mechanisms are not fully understood. Here, we aimed to investigate the effects of bromelain on non-alcoholic fatty liver disease (NAFLD)-induced deregulation of blood coagulation and the underlying molecular mechanisms. C57BL/6 mice were fed a high-fat diet (HFD), with or without bromelain (20 mg/kg/day) administration, for 12 weeks. Treatment with bromelain decreased thrombus formation in the liver and prolonged HFD-induced shortened prothrombin, activated partial thromboplastin, and fibrinogen times. Moreover, liquid chromatography-mass spectrometry/mass spectrometry and Western blot analysis showed that bromelain inhibited NAFLD-induced activation of the intrinsic, extrinsic, and common pathways by upregulating the protein expression of antithrombin III, serpin family G member 1, and α1-antitrypsin, and downregulating the protein expression of fibrinogen in the liver and plasma. Bromelain also upregulated the level of plasminogen and downregulating factor XIII expression in the liver and plasma. Collectively, these findings suggest that bromelain exerts anticoagulant effects on NAFLD-induced deregulation of coagulation by inhibiting the activation of the coagulation cascade, decreasing the stability of clots, and promoting fibrinolytic activity. The present study provides new insights into the potential therapeutic value of bromelain for the prevention and treatment of thrombosis-related diseases. Full article

(This article belongs to the Special Issue Functional Foods: Regulation of Metabolism from Molecule to System and Disease Control)

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18 pages, 6341 KiB

Open AccessArticle

Dioscin Ameliorates Hyperuricemia-Induced Atherosclerosis by Modulating of Cholesterol Metabolism through FXR-Signaling Pathway

by Ruixia Bao, Wei Wang, Beibei Chen, Jujie Pan, Qian Chen, Mengyang Liu, Dan Wang, Yuzheng Wu, Haiyang Yu, Lifeng Han, Yi Zhang and Tao Wang

Nutrients 2022, 14(9), 1983; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14091983 - 09 May 2022

Cited by 4 | Viewed by 2549

Abstract

Hyperuricemia is one of the independent risk factors for atherosclerotic cardiovascular disease. Herein, we investigate the association between uric acid and cholesterol metabolism and the effect of dioscin on the prevention of hyperuricemia-induced atherosclerosis. In the potassium oxonate-treated ApoE^{−/−−/−} mice, atherosclerosis was accelerated along with elevated serum cholesterol levels in the hyperuricemic state, which can be ameliorated by dioscin. Together with the in vitro assays, we found that the effect of dioscin was at least partially through the regulation of the farnesoid X receptor (FXR) -small heterodimer partner (SHP) -7α-hydroxylase (CYP7A1) signaling pathway in the liver. Tigogenin (a metabolite of dioscin) suppressed FXR activation and increased CYP7A1, resulting in an increased conversion rate of cholesterols into bile acids. Further clinical study revealed that treatment with a dioscin-enriched preparation decreased serum cholesterol levels in individuals with hyperuricemia. In summary, this study demonstrated a slowdown effect of dioscin on the progression of hyperuricemia-induced atherosclerosis. Full article

(This article belongs to the Special Issue Functional Foods: Regulation of Metabolism from Molecule to System and Disease Control)

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16 pages, 2063 KiB

Open AccessArticle

Fibroblast Growth Factor 19 and Fibroblast Growth Factor 21 Regulation in Obese Diabetics, and Non-Alcoholic Fatty Liver Disease after Gastric Bypass

by Jiun-Yu Guo, Hsin-Hung Chen, Wei-Jei Lee, Shu-Chun Chen, Shou-Dong Lee and Chih-Yen Chen

Nutrients 2022, 14(3), 645; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14030645 - 02 Feb 2022

Cited by 10 | Viewed by 2132

Abstract

Background: Gastric bypass (GB) is an effective treatment for those who are morbidly obese with coexisting type 2 diabetes mellitus (T2DM) or non-alcoholic fatty liver disease (NAFLD). Fibroblast growth factors (FGFs) are involved in the regulation of energy metabolism. Methods: We investigated the roles of FGF 19, FGF 21, and total bile acid among those with morbidly obese and T2DM undergoing GB. A total of 35 patients were enrolled. Plasma FGF 19, FGF 21, and total bile acid levels were measured before surgery (M0), 3 months (M3), and 12 months (M12) after surgery, while the hepatic steatosis index (HSI) was calculated before and after surgery. Results: Obese patients with T2DM after GB presented with increased serum FGF 19 levels (p = 0.024) and decreased total bile acid (p = 0.01) and FGF 21 levels (p = 0.005). DM complete remitters had a higher FGF 19 level at M3 (p = 0.004) compared with DM non-complete remitters. Fatty liver improvers tended to have lower FGF 21 (p = 0.05) compared with non-improvers at M12. Conclusion: Changes in FGF 19 and FGF 21 play differential roles in DM remission and NAFLD improvement for patients after GB. Early increases in serum FGF 19 levels may predict complete remission of T2DM, while a decline in serum FGF 21 levels may reflect the improvement of NAFLD after GB. Full article

(This article belongs to the Special Issue Functional Foods: Regulation of Metabolism from Molecule to System and Disease Control)

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8 pages, 236 KiB

Open AccessArticle

ApoE4 Is Associated with Lower Body Mass, Particularly Fat Mass, in Older Women with Cognitive Impairment

by Takafumi Ando, Kazuaki Uchida, Taiki Sugimoto, Ai Kimura, Naoki Saji, Shumpei Niida and Takashi Sakurai

Nutrients 2022, 14(3), 539; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14030539 - 26 Jan 2022

Cited by 6 | Viewed by 2719

Abstract

A lower body mass is associated with the progression of Alzheimer’s disease (AD) and the risk of mortality in patients with AD; however, evidence of genetic determinants of decreased body mass in cognitively impaired older adults is limited. We therefore investigated the genetic effect of APOE-ε4 on body composition in older adults with mild cognitive impairment (MCI) and early-to-moderate-stage AD. A total of 1631 outpatients (aged 65–89 years) with MCI and early-to-moderate-stage AD were evaluated for the association between body composition and APOE-ε4 status. After adjusting for covariates, including cognitive function evaluated with the Mini-Mental State Examination, the presence of the APOE-ε4 was associated with lower weight (β = −1.116 ± 0.468 kg per presence, p = 0.017), fat mass (β = −1.196 ± 0.401 kg per presence, p = 0.003), and percentage of body fat (β = −1.700 ± 0.539% per presence, p = 0.002) in women but not in men. Additionally, the impact of APOE-ε4 on measures of body composition in women was more remarkable in MCI than in AD patients. The presence of the APOE-ε4 allele was associated with lower fat mass, particularly in women with MCI, independent of cognitive decline. Full article

(This article belongs to the Special Issue Functional Foods: Regulation of Metabolism from Molecule to System and Disease Control)

11 pages, 11824 KiB

Open AccessArticle

Circadian Clock Component BMAL1 in the Paraventricular Nucleus Regulates Glucose Metabolism

by Masanori Nakata, Parmila Kumari, Rika Kita, Nanako Katsui, Yuriko Takeuchi, Tomoki Kawaguchi, Toshiya Yamazaki, Boyang Zhang, Shigeki Shimba and Toshihiko Yada

Nutrients 2021, 13(12), 4487; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13124487 - 15 Dec 2021

Cited by 12 | Viewed by 3018

Abstract

It is suggested that clock genes link the circadian rhythm to glucose and lipid metabolism. In this study, we explored the role of the clock gene Bmal1 in the hypothalamic paraventricular nucleus (PVN) in glucose metabolism. The Sim1-Cre-mediated deletion of Bmal1 markedly reduced insulin secretion, resulting in impaired glucose tolerance. The pancreatic islets’ responses to glucose, sulfonylureas (SUs) and arginine vasopressin (AVP) were well maintained. To specify the PVN neuron subpopulation targeted by Bmal1, the expression of neuropeptides was examined. In these knockout (KO) mice, the mRNA expression of Avp in the PVN was selectively decreased, and the plasma AVP concentration was also decreased. However, fasting suppressed Avp expression in both KO and Cre mice. These results demonstrate that PVN BMAL1 maintains Avp expression in the PVN and release to the circulation, possibly providing islet β-cells with more AVP. This action helps enhance insulin release and, consequently, glucose tolerance. In contrast, the circadian variation of Avp expression is regulated by feeding, but not by PVN BMAL1. Full article

(This article belongs to the Special Issue Functional Foods: Regulation of Metabolism from Molecule to System and Disease Control)

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18 pages, 4547 KiB

Open AccessArticle

Astaxanthin, a Marine Carotenoid, Maintains the Tolerance and Integrity of Adipose Tissue and Contributes to Its Healthy Functions

by Allah Nawaz, Yasuhiro Nishida, Akiko Takikawa, Shiho Fujisaka, Tomonobu Kado, Aminuddin Aminuddin, Muhammad Bilal, Ishtiaq Jeelani, Muhammad Rahil Aslam, Ayumi Nishimura, Takahide Kuwano, Yoshiyuki Watanabe, Yoshiko Igarashi, Keisuke Okabe, Saeed Ahmed, Azhar Manzoor, Isao Usui, Kunimasa Yagi, Takashi Nakagawa and Kazuyuki Tobe

Nutrients 2021, 13(12), 4374; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13124374 - 06 Dec 2021

Cited by 6 | Viewed by 4347

Abstract

Recently, obesity-induced insulin resistance, type 2 diabetes, and cardiovascular disease have become major social problems. We have previously shown that Astaxanthin (AX), which is a natural antioxidant, significantly ameliorates obesity-induced glucose intolerance and insulin resistance. It is well known that AX is a strong lipophilic antioxidant and has been shown to be beneficial for acute inflammation. However, the actual effects of AX on chronic inflammation in adipose tissue (AT) remain unclear. To observe the effects of AX on AT functions in obese mice, we fed six-week-old male C57BL/6J on high-fat-diet (HFD) supplemented with or without 0.02% of AX for 24 weeks. We determined the effect of AX at 10 and 24 weeks of HFD with or without AX on various parameters including insulin sensitivity, glucose tolerance, inflammation, and mitochondrial function in AT. We found that AX significantly reduced oxidative stress and macrophage infiltration into AT, as well as maintaining healthy AT function. Furthermore, AX prevented pathological AT remodeling probably caused by hypoxia in AT. Collectively, AX treatment exerted anti-inflammatory effects via its antioxidant activity in AT, maintained the vascular structure of AT and preserved the stem cells and progenitor’s niche, and enhanced anti-inflammatory hypoxia induction factor-2α-dominant hypoxic response. Through these mechanisms of action, it prevented the pathological remodeling of AT and maintained its integrity. Full article

(This article belongs to the Special Issue Functional Foods: Regulation of Metabolism from Molecule to System and Disease Control)

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12 pages, 1203 KiB

Open AccessArticle

Repeated Oral Administration of Flavan-3-ols Induces Browning in Mice Adipose Tissues through Sympathetic Nerve Activation

by Yuko Ishii, Orie Muta, Tomohiro Teshima, Nayuta Hirasima, Minayu Odaka, Taiki Fushimi, Yasuyuki Fujii and Naomi Osakabe

Nutrients 2021, 13(12), 4214; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13124214 - 24 Nov 2021

Cited by 5 | Viewed by 9458

Abstract

We previously found increases in uncoupling protein (Ucp)-1 transcription in brown adipose tissue (BAT) of mice following a single oral dose of flavan 3-ol (FL)s, a fraction of catechins and procyanidins. It was confirmed that these changes were totally reduced by co-treatment of adrenaline blockers. According to these previous results, FLs possibly activate sympathetic nervous system (SNS). In this study, we confirmed the marked increase in urinary catecholamine (CA) s projecting SNS activity following a single dose of 50 mg/kg FLs. In addition, we examined the impact of the repeated administration of 50 mg/kg FLs for 14 days on adipose tissues in mice. In BAT, FLs tended to increase the level of Ucp-1 along with significant increase of thermogenic transcriptome factors expressions, such as peroxisome proliferator-activated receptor γ coactivator (PGC)-1α and PR domain-containing (PRDM)1. Expression of browning markers, CD137 and transmembrane protein (TMEM) 26, in addition to PGC-1α were increased in epididymal adipose (eWAT) by FLs. A multilocular morphology with cell size reduction was shown in the inguinal adipose (iWAT), together with increasing the level of Ucp-1 by FLs. These results exert that FLs induce browning in adipose, and this change is possibly produced by the activation of the SNS. Full article

(This article belongs to the Special Issue Functional Foods: Regulation of Metabolism from Molecule to System and Disease Control)

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Review

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39 pages, 2336 KiB

Open AccessReview

Astaxanthin as a Novel Mitochondrial Regulator: A New Aspect of Carotenoids, beyond Antioxidants

by Yasuhiro Nishida, Allah Nawaz, Karen Hecht and Kazuyuki Tobe

Nutrients 2022, 14(1), 107; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14010107 - 27 Dec 2021

Cited by 33 | Viewed by 7293

Abstract

Astaxanthin is a member of the carotenoid family that is found abundantly in marine organisms, and has been gaining attention in recent years due to its varied biological/physiological activities. It has been reported that astaxanthin functions both as a pigment, and as an antioxidant with superior free radical quenching capacity. We recently reported that astaxanthin modulated mitochondrial functions by a novel mechanism independent of its antioxidant function. In this paper, we review astaxanthin’s well-known antioxidant activity, and expand on astaxanthin’s lesser-known molecular targets, and its role in mitochondrial energy metabolism. Full article

(This article belongs to the Special Issue Functional Foods: Regulation of Metabolism from Molecule to System and Disease Control)

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