Reduced adiponectin expression after high‐fat diet is associated with selective up‐regulation of ALDH1A1 and further retinoic acid receptor signaling in adipose tissue

Landrier, Jean‐François; Kasiri, Elnaz; Karkeni, Esma; Mihály, Johanna; Béke, Gabriella; Weiss, Kathrin; Lucas, Renata; Aydemir, Gamze; Salles, Jérôme; Walrand, Stéphane; Lera, Ángel R. de; Rühl, Ralph

doi:10.1096/fj.201600263rr

Cited by 45 publications

(42 citation statements)

References 86 publications

(130 reference statements)

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“…Previous studies reported that low levels of adiponectin in serum can be a strong predictor for MetS (Kim et al 2013), insulin resistance (Awazawa et al 2011) and type 2 diabetes (Yamamoto et al 2014). Previous studies reported the reductions in adiponectin gene and protein expression under high-fat dietary condition in animals (Barnea et al 2006;Landrier et al 2017). Congruent with these past findings, our results demonstrated that the animals with MetS induced by HCHF diet had a lower level of adiponectin compared to the normal control animals.…”

Section: Discussionsupporting

confidence: 81%

Leptin, Adiponectin and Insulin as Regulators for Energy Metabolism in a Rat Model of Metabolic Syndrome

Wong¹,

Chin²,

Ima‐Nirwana³

2019

JSM

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Leptin, adiponectin, and insulin are pivotal regulators for lipid and glucose metabolism. This study aimed to investigate the changes in these hormones in a rat model of metabolic syndrome (MetS) induced by high-carbohydrate high-fat (HCHF) diet. Twelve-week-old male Wistar rats were divided into two experimental groups. The normal group was given standard rat chow with tap water. The HCHF group was given HCHF diet with 25% fructose-supplemented drinking water to induce MetS. Body composition of the animals was measured using dual-energy X-ray absorptiometry. Blood was collected at week 0, 8, 12, and 16 for the measurement of blood glucose and hormone levels. Our findings demonstrated that HCHF diet significantly increased fat mass, percentage of fat, and decreased lean mass in the animals starting from week 8. The levels of blood glucose, leptin, and insulin were significantly higher but the level of adiponectin was significantly lower in the HCHF rats compared to the normal rats. In conclusion, hormones play a key underlying role in regulating lipid and glucose metabolism in MetS.

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Section: Discussionsupporting

confidence: 81%

Leptin, Adiponectin and Insulin as Regulators for Energy Metabolism in a Rat Model of Metabolic Syndrome

Wong¹,

Chin²,

Ima‐Nirwana³

2019

JSM

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“…Dietary transglutaminases can provide PPAR ligands, thus synchronising fat, and concomitantly carotenoid, uptake / availability with BCO1 up-regulation. It was described that the main BCO1-metabolite ATRA is regulating via ATRA-RAR-mediated signalling various important steps in lipid metabolism (206,225,226) , with β-Carotene bioactivation pathway a focus also on counteracting fat accumulation via energy dissipation in adipose tissue (226)(227)(228)(229) and regulation of insulin secretion (230,231) . The second possibility for negative feedback is the potential synthesis of the endogenous RXR-ligand 9CDHRA, starting from still non-identified carotenoid precursors (Rühl et al, unpublished results (160) ).…”

Section: β-Carotene Bioactivation Pathway 77mentioning

confidence: 99%

β-Carotene in the human body: metabolic bioactivation pathways – from digestion to tissue distribution and excretion

et al. 2019

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5Paprika Bioanalytics BT, Debrecen, Hungary β-Carotene intake and tissue/blood concentrations have been associated with reduced incidence of several chronic diseases. Further bioactive carotenoid-metabolites can modulate the expression of specific genes mainly via the nuclear hormone receptors: retinoic acid receptor-and retinoid X receptor-mediated signalling. To better understand the metabolic conversion of β-carotene, inter-individual differences regarding β-carotene bioavailability and bioactivity are key steps that determine its further metabolism and bioactivation and mediated signalling. Major carotenoid metabolites, the retinoids, can be stored as esters or further oxidised and excreted via phase 2 metabolism pathways. In this review, we aim to highlight the major critical control points that determine the fate of β-carotene in the human body, with a special emphasis on β-carotene oxygenase 1. The hypothesis that higher dietary β-carotene intake and serum level results in higher β-carotene-mediated signalling is partly questioned. Alternative autoregulatory mechanisms in β-carotene / retinoid-mediated signalling are highlighted to better predict and optimise nutritional strategies involving βcarotene-related health beneficial mediated effects.

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“…Adipose tissue and in particular the lipid fraction of adipocytes is an important site of carotenoid accumulation . Vitamin A is stored in adipose tissue primarily as unesterified retinol . Concentrations of carotenoids in adipose tissue have been reported by several groups (Table ).…”

Section: Further Transport and Biodistribution To Potential Target Timentioning

confidence: 99%

Host‐related factors explaining interindividual variability of carotenoid bioavailability and tissue concentrations in humans

Bohn

Desmarchelier

Dragsted

et al. 2017

Molecular Nutrition Food Res

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196

159

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Carotenoid dietary intake and their endogenous levels have been associated with a decreased risk of several chronic diseases. There are indications that carotenoid bioavailability depends, in addition to the food matrix, on host factors. These include diseases (e.g. colitis), life‐style habits (e.g. smoking), gender and age, as well as genetic variations including single nucleotide polymorphisms that govern carotenoid metabolism. These are expected to explain interindividual differences that contribute to carotenoid uptake, distribution, metabolism and excretion, and therefore possibly also their association with disease risk. For instance, digestion enzymes fostering micellization (PNLIP, CES), expression of uptake/efflux transporters (SR‐BI, CD36, NPC1L1), cleavage enzymes (BCO1/2), intracellular transporters (FABP2), secretion into chylomicrons (APOB, MTTP), carotenoid metabolism in the blood and liver (LPL, APO C/E, LDLR), and distribution to target tissues such as adipose tissue or macula (GSTP1, StARD3) depend on the activity of these proteins. In addition, human microbiota, e.g. via altering bile‐acid concentrations, may play a role in carotenoid bioavailability. In order to comprehend individual, variable responses to these compounds, an improved knowledge on intra‐/interindividual factors determining carotenoid bioavailability, including tissue distribution, is required. Here, we highlight the current knowledge on factors that may explain such intra‐/interindividual differences.

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Reduced adiponectin expression after high‐fat diet is associated with selective up‐regulation of ALDH1A1 and further retinoic acid receptor signaling in adipose tissue

Cited by 45 publications

References 86 publications

Leptin, Adiponectin and Insulin as Regulators for Energy Metabolism in a Rat Model of Metabolic Syndrome

Leptin, Adiponectin and Insulin as Regulators for Energy Metabolism in a Rat Model of Metabolic Syndrome

β-Carotene in the human body: metabolic bioactivation pathways – from digestion to tissue distribution and excretion

Host‐related factors explaining interindividual variability of carotenoid bioavailability and tissue concentrations in humans

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