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BACKGROUND: Obesity leads to chronic low-grade inflammation, promoting detrimental effects on bone. The consumption of virgin coconut oil (VCO) is associated with benefits related to meta-inflammation. We evaluated the effect of VCO supplementation on osteopenia promoted by diet-induced obesity in mice. METHODS: Male BALB/c mice were fed a control (C) or highly refined carbohydrate-containing (HC) diet for eight weeks. After that, the HC diet group was supplemented with three doses of VCO for four weeks. RESULTS: The HC diet increased the adiposity and leptin levels associated with augmented systemic inflammatory cells improved with VCO supplementation. The HC diet reduced the trabecular bone in the tibia, lumbar vertebrae, distal and proximal femur, as well as the bone mineral density of the femur and alveolar bone. The VCO supplementation reverted bone osteopenia by increasing the trabecular bone in different sites and improving femur and alveolar bone microarchitecture. Although the reduced number of osteoblasts in the alveolar bone of the HC diet group was not significantly enhanced by VCO supplementation, the reduced Alp expression in the HC diet group was enhanced in the VCO group. These beneficial effects were associated with lowering the Rankl/Opg ratio. CONCLUSION: VCO supplementation might be an effective strategy to attenuate bone osteopenic effects induced by obesity.

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A obesidade é caracterizada pelo acúmulo de gordura corporal associada a uma inflamação crônica de baixo grau, sendo relacionada ao aumento do risco para o desenvolvimento de perda óssea, e consequentemente osteoporose. A perda óssea acontece devido a diversos fatores, dentre eles a presença de resposta inflamatória. As doenças crônicas como a obesidade apresentam aumento na síntese e secreção de mediadores inflamatórios que poderiam favorecer a perda óssea. Apesar de abordagens dietéticas serem propostas para tratar a perda óssea, elas ainda são pouco exploradas. O óleo de coco virgem (OCV) é um alimento funcional devido à sua quantidade significativa de ácidos graxos de cadeia média. Nos últimos anos, o OCV tem sido amplamente utilizado como possível tratamento de diversas doenças incluindo Alzheimer, doenças cardíacas, obesidade, entre outras. Contudo, conhecimentos a respeito da suplementação com OCV no tratamento da perda óssea ainda é incipiente. Esse estudo objetivou avaliar o efeito da suplementação dietética com OCV no tratamento na perda óssea de camundongos alimentados com dieta rica em gordura 45% (HF). Camundongos machos C57BL/6 foram inicialmente divididos em dois grupos e alimentados com dieta controle AIN-93M (C) ou dieta HF por oito semanas. Na 9ª semana, os camundongos alimentados com dieta HF foram reagrupados em quatro grupos até a 12ª semana: (i) dieta HF; ou dieta HF suplementada com diferentes doses de OCV, (iii) 1000 mg/kg, (iv) 3000 mg/kg ou (v) 9000 mg/kg. Apesar do ganho de peso não apresentar diferença estatística entre os grupos, o peso corporal final foi maior no grupo HF em relação ao grupo controle, mas sem alteração naqueles tratados com OCV em relação ao controle. Não houve diferença significativa na ingestão alimentar entre os grupos avaliados. Ao serem avaliados parâmetros ósseos, as concentrações séricas de RANKL, um marcador de perda óssea, e OPG, opositora a essa sinalização, não se alteraram entre os grupos. Contudo, somente os animais que receberam a dose média de OCV apresentaram tendência para menor relação RANKL/OPG, sendo essa a dose escolhida para a avaliação da microarquitetura óssea. No geral, o grupo HF apresentou menor densidade mineral óssea e volume ósseo, trabéculas de menor espessura com maior espaço entre elas, caracterizando aumento da reabsorção óssea na estrutura óssea do fêmur e maxila. Quando tratados com a dose média de OCV ocorreu uma piora da densidade mineral óssea e da separação trabéculas na maxila, sem alteração nos outros parâmetros quando comparados com o grupo HF. Contudo, a perda óssea presente no fêmur não foi alterada. Como esperado, a adiposidade, área de adipócitos e concentrações séricas de leptina foram maiores no grupo alimentado com dieta HF em relação ao controle. No grupo tratado com a dose alta de OCV foi observado um aumento da área dos adipócitos, mas nos demais parâmetros não foram observadas alterações após os diferentes tratamentos com o OCV. A intolerância à glicose observada no grupo HF não foi alterada com a adição do OCV à dieta HF, e ainda se mostraram hiperglicêmicos. Apesar de alteradas no grupo HF, as concentrações séricas de colesterol total e triglicérides não se modificaram com os tratamentos. Portanto, o uso da suplementação com OCV em camundongos alimentados com a dieta HF parece não ser benéfico para tratar perda óssea, a obesidade e ainda as disfunções metabólicas associadas.

Obesity is characterized by the accumulation of body fat associated with low-grade chronic inflammation, which is related to an increased risk of developing bone loss, and consequently, osteoporosis. Bone loss occurs due to several factors, including the presence of an inflammatory response. Chronic diseases such as obesity show an increase in the synthesis and secretion of inflammatory mediators that could favor bone loss. Although dietary approaches are proposed to treat bone loss, they are still poorly explored. Virgin coconut oil (VCO) is a functional food due to its significant amount of medium-chain fatty acids. In recent years, VCO has been widely used to treat several diseases, including Alzheimer's, heart disease, obesity, among others. However, knowledge about VCO supplementation in the treatment of bone loss is still incipient. This study aimed to evaluate the effect of dietary supplementation with VCO in the treatment of bone loss in mice fed a 45% high-fat (HF) diet. Male C57BL / 6 mice were initially divided into two groups and fed either the AIN-93M (C) control diet or the HF diet for eight weeks. At the 9th week, the mice fed the HF diet were regrouped in four groups until the 12th week: (i) HF diet; or HF diet supplemented with different doses of VCO, (iii) 1000 mg / kg, (iv) 3000 mg / kg or (v) 9000 mg / kg. Although the weight gain does not present a statistical difference between the groups, the final body weight was higher in the HF group than the control group, but without changes in those treated with VCO in relation to the control. There was no significant difference in food intake between the groups evaluated. When bone parameters were evaluated, the serum concentrations of RANKL, a bone loss marker, and OPG, opposed to this signaling, did not change between the groups. However, only animals that received the medium dose of VCO showed a tendency towards a lower RANKL / OPG ratio, which was the dose chosen for bone microarchitecture evaluation. In general, the HF group showed lower bone mineral density and bone volume, thinner trabeculae with greater space between them, characterizing increased bone resorption in the femur and maxilla's bone structure. When treated with the medium dose of VCO, there was a worsening of bone mineral density and trabecular separation in the maxilla, with no change in other parameters when compared with the HF group. However, the bone loss present in the femur was not altered. As expected, adiposity, area of adipocytes and serum leptin concentrations were higher in the group fed with HF compared to the control group. In the group treated with the high dose of VCO an increase in the area of adipocytes was observed, but in the other parameters, no changes were observed after the different treatments with the VCO. The glucose intolerance observed in the HF group was not altered with the addition of VCO to the HF diet, and they were also shown to be hyperglycemic. Despite being changed in the HF group, serum concentrations of total cholesterol and triglycerides did not change with treatments. Therefore, the use of VCO supplementation in mice fed the HF diet does not seem to be beneficial for treating bone loss, obesity, and even the associated metabolic disorders.

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The global rise in obesity rates is alarming since this condition is associated with chronic low-grade inflammation and secondary comorbidities as glucose intolerance, cardiovascular disease and liver damage. Therefore, a lot of dietary approaches are proposed to prevent and to treat obesity and its associated disorders. Virgin coconut oil (VCO) is well known as a functional food due to its significant amounts of medium-chain triglycerides. This study aimed to evaluate the effect of VCO on adiposity, metabolic and inflammatory dysfunctions induced by a high-refined carbohydrate-containing (HC) diet in mice. Male BALB/c mice were divided into two groups and fed with control (C) or HC diet to induce obesity for eight weeks. At the 9th week mice fed with HC diet were randomly regrouped into four groups, and were kept this way until the 12th week, as following: (i) HC diet alone or HC diet supplemented with three different VCO doses (ii) 1000 mg/kg, (iii) 3000 mg/kg and (iv) 9000 mg/kg. Regardless of the concentration used, VCO supplementation promoted lower adiposity and also improvement in glucose tolerance, lower serum glucose and lipid levels and decreased hepatic steatosis. Moreover, VCO intake induced a lower inflammatory response due to decreased number of leukocytes and TNF-α and IL-6 concentrations in adipose tissue, as well as reduced counts of total leukocytes, mononuclear and polymorphonuclear circulating cells. Our data showed that VCO can be considered as an interesting potential dietary approach to attenuate obesity and its metabolic and inflammatory alterations.

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This study evaluated the effects of a ketogenic diet (KD) based on extra virgin coconut oil (Cocos nucifera L., VCO), on the treatment of epileptic rats. Two sets of experiments were conducted. First, male Wistar rats underwent induction of status epilepticus (SE) with the administration of pilocarpine intraperitoneally 21 animals reached spontaneous recurrent seizures (SRS) and were randomly allocated to the dietary regimens and video-monitored for 19 days. In the second experiment, 24 animals were randomized immediately after the induction of SE and followed for 67 days. Diets were as follows: Control (AIN-93G; 7% lipid), KetoTAGsoya (KD based on soybean oil; 69.79% lipid), and KetoTAGcoco (KD based on VCO; 69.79% lipid). There were no differences in the latency to the first crisis, total frequency, and duration of the SRS between groups in 2 experiments. The data suggest no effects of KD, with or without VCO, in rats with pilocarpine-induced epilepsy.

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ABSTRACT: This study aimed to evaluate the influence of replacing soybean oil with extra virgin coconut oil in normolipidic and hyperlipidic diets, on the lipid metabolism of Wistar rats. In the first stage of the experiment (30 days), 36 rats were divided into 2 groups and fed with a control or a hyperlipidic diet. Six animals from each group were then killed, and the remaining rats were redistributed into 4 new groups: 2 groups remained on the control and hyperlipidic diets, and in the diets of the other 2 groups, the soybean oil was replaced with coconut oil (30 days). At the end of the assay, the biological models were decapitated for blood collection and removal of organs and peritoneal fat. Although the diet intake differed among groups during both stages of the experiment, no differences were noted with regard to weight gain and peritoneal fat. Replacing soybean oil with coconut oil in the rat diet lowered triglyceride and low-density lipoprotein serum concentrations in both groups. Liver parameters, namely, total cholesterol and triacylglycerols, increased with the substitution of soybean oil by coconut oil in the normolipidic diet and decreased in the hyperlipidic diet. Thus, replacing soybean oil by coconut oil may improve serum and liver lipid levels in Wistar rats.

RESUMO: O estudo teve como objetivo avaliar a influência da substituição do óleo de soja por óleo de coco extravirgem em dietas normolipídicas e hiperlipídicas, sobre o metabolismo lipídico de ratos Wistar. Na primeira fase do experimento, 30 dias, 36 ratos foram distribuídos em dois grupos, receberam dieta controle e dieta hiperlipídica. Após eutanásia de seis animais por grupo, os ratos de ambos os grupos foram redistribuídos em quatro novos grupos, dois permaneceram com as dietas controle e hiperlipídica e nos outros dois houve substituição do óleo de soja por óleo de coco (30 dias). Ao final do ensaio, os modelos biológicos foram decapitados, para coleta de sangue, retirada de órgãos e gordura peritoneal. O consumo de dieta foi diferente entre os grupos durante as duas fases do experimento, porém sem diferença no ganho de peso e gordura peritoneal. A substituição, na dieta, do óleo de soja por óleo de coco diminuiu as concentrações séricas de triacilgliceróis e de lipoproteínas de baixa densidade, em ambos os grupos. Os parâmetros hepáticos colesterol total e triacilgliceróis aumentaram com a substituição do óleo de soja por óleo de coco em dieta normolipídica e diminuíram na dieta hiperlipídica. A substituição do óleo de soja por óleo de coco pode ter benefícios com relação aos lipídeos séricos e hepáticos em ratos Wistar.

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This study aimed to evaluate the influence of replacing soybean oil with extra virgin coconut oil in normolipidic and hyperlipidic diets, on the lipid metabolism of Wistar rats. In the first stage of the experiment (30 days), 36 rats were divided into 2 groups and fed with a control or a hyperlipidic diet. Six animals from each group were then killed, and the remaining rats were redistributed into 4 new groups: 2 groups remained on the control and hyperlipidic diets, and in the diets of the other 2 groups, the soybean oil was replaced with coconut oil (30 days). At the end of the assay, the biological models were decapitated for blood collection and removal of organs and peritoneal fat. Although the diet intake differed among groups during both stages of the experiment, no differences were noted with regard to weight gain and peritoneal fat. Replacing soybean oil with coconut oil in the rat diet lowered triglyceride and low-density lipoprotein serum concentrations in both groups. Liver parameters, namely, total cholesterol and triacylglycerols, increased with the substitution of soybean oil by coconut oil in the normolipidic diet and decreased in the hyperlipidic diet. Thus, replacing soybean oil by coconut oil may improve serum and liver lipid levels in Wistar rats.(AU)

O estudo teve como objetivo avaliar a influência da substituição do óleo de soja por óleo de coco extravirgem em dietas normolipídicas e hiperlipídicas, sobre o metabolismo lipídico de ratos Wistar. Na primeira fase do experimento, 30 dias, 36 ratos foram distribuídos em dois grupos, receberam dieta controle e dieta hiperlipídica. Após eutanásia de seis animais por grupo, os ratos de ambos os grupos foram redistribuídos em quatro novos grupos, dois permaneceram com as dietas controle e hiperlipídica e nos outros dois houve substituição do óleo de soja por óleo de coco (30 dias). Ao final do ensaio, os modelos biológicos foram decapitados, para coleta de sangue, retirada de órgãos e gordura peritoneal. O consumo de dieta foi diferente entre os grupos durante as duas fases do experimento, porém sem diferença no ganho de peso e gordura peritoneal. A substituição, na dieta, do óleo de soja por óleo de coco diminuiu as concentrações séricas de triacilgliceróis e de lipoproteínas de baixa densidade, em ambos os grupos. Os parâmetros hepáticos colesterol total e triacilgliceróis aumentaram com a substituição do óleo de soja por óleo de coco em dieta normolipídica e diminuíram na dieta hiperlipídica. A substituição do óleo de soja por óleo de coco pode ter benefícios com relação aos lipídeos séricos e hepáticos em ratos Wistar.(AU)

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The hypothesis that oral supplementation with virgin coconut oil (Cocos nucifera L.) and exercise training would improve impaired baroreflex sensitivity (BRS) and reduce oxidative stress in spontaneously hypertensive rats (SHR) was tested. Adult male SHR and Wistar Kyoto rats (WKY) were divided into 5 groups: WKY + saline (n = 8); SHR + saline (n = 8); SHR + coconut oil (2 mL·day(-1), n = 8); SHR + trained (n = 8); and SHR + trained + coconut oil (n = 8). Mean arterial pressure (MAP) was recorded and BRS was tested using phenylephrine (8 µg/kg, intravenous) and sodium nitroprusside (25 µg·kg(-1), intravenous). Oxidative stress was measured using dihydroethidium in heart and aorta. SHR + saline, SHR + coconut oil, and SHR + trained group showed higher MAP compared with WKY + saline (175 ± 6, 148 ± 6, 147 ± 7 vs. 113 ± 2 mm Hg; p < 0.05). SHR + coconut oil, SHR + trained group, and SHR + trained + coconut oil groups presented lower MAP compared with SHR + saline group (148 ± 6, 147 ± 7, 134 ± 8 vs. 175 ± 6 mm Hg; p < 0.05). Coconut oil combined with exercise training improved BRS in SHR compared with SHR + saline group (-2.47 ± 0.3 vs. -1.39 ± 0.09 beats·min(-1)·mm Hg(-1); p < 0.05). SHR + saline group showed higher superoxide levels when compared with WKY + saline (774 ± 31 vs. 634 ± 19 arbitrary units (AU), respectively; p < 0.05). SHR + trained + coconut oil group presented reduced oxidative stress compared with SHR + saline in heart (622 ± 16 vs. 774 ± 31 AU, p < 0.05). In aorta, coconut oil reduced oxidative stress in SHR compared with SHR + saline group (454 ± 33 vs. 689 ± 29 AU, p < 0.05). Oral supplementation with coconut oil combined with exercise training improved impaired BRS and reduced oxidative stress in SHR.

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