Olive leaf extract prevents obesity, cognitive decline, and depression and improves exercise capacity in mice

Mikami, Toshio; Kim, Jimmy; Park, Jong-Hyuk; Lee, Hyowon; Yaicharoen, Pongson; Suidasari, Sofya; Yokozawa, Miki; Yamauchi, Ken

doi:10.1038/s41598-021-90589-6

Cited by 15 publications

(6 citation statements)

References 59 publications

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“…The results demonstrate that high-intensity exercise or lactate administration increases hippocampal extracellular lactate concentration, which could induce hippocampal PGC-1α mRNA expression and increase mtDNA copy number. Moreover, hippocampal BDNF mRNA expression was also increased after a single bout of high-intensity exercise, which was consistent with a previous study showing that increased PGC-1α led to the induction of BDNF expression ( Wrann et al, 2013 ; Mikami et al, 2021 ). In addition, the lactate-induced hippocampal BDNF expression was suppressed by injecting MCT1/2 inhibitor, AR-C155858 ( El Hayek et al, 2019 ).…”

Section: Discussionsupporting

confidence: 92%

“…For quantifying hippocampal mtDNA, total DNA was extracted from the hippocampus using the phenol-chloroform method, as described previously (Mikami et al, 2021). First, the hippocampal tissue (~20 mg) was dissolved in 200 μl of lysate buffer containing 10 mM Tris-HCl (pH 8.0), 150 mM NaCl, 10 mM EDTA (pH 8.0), 0.1% SDS, and 2.5% proteinase K; next, it was vortexed, incubated at 56°C for 90 min, and centrifuged at 2,000 g for 10 min.…”

Section: Mtdna Copy Numbermentioning

confidence: 99%

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Exercise-Induced Lactate Release Mediates Mitochondrial Biogenesis in the Hippocampus of Mice via Monocarboxylate Transporters

2021

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Regular exercise training induces mitochondrial biogenesis in the brain via activation of peroxisome proliferator-activated receptor gamma-coactivator 1α (PGC-1α). However, it remains unclear whether a single bout of exercise would increase mitochondrial biogenesis in the brain. Therefore, we first investigated whether mitochondrial biogenesis in the hippocampus is affected by a single bout of exercise in mice. A single bout of high-intensity exercise, but not low- or moderate-intensity, increased hippocampal PGC-1α mRNA and mitochondrial DNA (mtDNA) copy number at 12 and 48h. These results depended on exercise intensity, and blood lactate levels observed immediately after exercise. As lactate induces mitochondrial biogenesis in the brain, we examined the effects of acute lactate administration on blood and hippocampal extracellular lactate concentration by in vivo microdialysis. Intraperitoneal (I.P.) lactate injection increased hippocampal extracellular lactate concentration to the same as blood lactate level, promoting PGC-1α mRNA expression in the hippocampus. However, this was suppressed by administering UK5099, a lactate transporter inhibitor, before lactate injection. I.P. UK5099 administration did not affect running performance and blood lactate concentration immediately after exercise but attenuated exercise-induced hippocampal PGC-1α mRNA and mtDNA copy number. In addition, hippocampal monocarboxylate transporters (MCT)1, MCT2, and brain-derived neurotrophic factor (BDNF) mRNA expression, except MCT4, also increased after high-intensity exercise, which was abolished by UK5099 administration. Further, injection of 1,4-dideoxy-1,4-imino-D-arabinitol (glycogen phosphorylase inhibitor) into the hippocampus before high-intensity exercise suppressed glycogen consumption during exercise, but hippocampal lactate, PGC-1α, MCT1, and MCT2 mRNA concentrations were not altered after exercise. These results indicate that the increased blood lactate released from skeletal muscle may induce hippocampal mitochondrial biogenesis and BDNF expression by inducing MCT expression in mice, especially during short-term high-intensity exercise. Thus, a single bout of exercise above the lactate threshold could provide an effective strategy for increasing mitochondrial biogenesis in the hippocampus.

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Section: Discussionsupporting

confidence: 92%

Section: Mtdna Copy Numbermentioning

confidence: 99%

Exercise-Induced Lactate Release Mediates Mitochondrial Biogenesis in the Hippocampus of Mice via Monocarboxylate Transporters

2021

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“…The study by Anders et al showed HFD could exacerbate depressive-like behaviors in the Flinders Sensitive Line (FSL) rat [ 43 ]. Another study also suggested that olive leaf extract may prevent depression by inhibiting fat mass and weight gain in mice fed with a high-fat diet [ 44 ].…”

Section: Overdose or Deficiency Of Macronutrients Elements Increase T...mentioning

confidence: 99%

Appropriate Macronutrients or Mineral Elements Are Beneficial to Improve Depression and Reduce the Risk of Depression

Zhengyang

Quan

et al. 2023

IJMS

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Depression is a common mental disorder that seriously affects the quality of life and leads to an increasing global suicide rate. Macro, micro, and trace elements are the main components that maintain normal physiological functions of the brain. Depression is manifested in abnormal brain functions, which are considered to be tightly related to the imbalance of elements. Elements associated with depression include glucose, fatty acids, amino acids, and mineral elements such as lithium, zinc, magnesium, copper, iron, and selenium. To explore the relationship between these elements and depression, the main literature in the last decade was mainly searched and summarized on PubMed, Google Scholar, Scopus, Web of Science, and other electronic databases with the keywords “depression, sugar, fat, protein, lithium, zinc, magnesium, copper, iron, and selenium”. These elements aggravate or alleviate depression by regulating a series of physiological processes, including the transmission of neural signals, inflammation, oxidative stress, neurogenesis, and synaptic plasticity, which thus affect the expression or activity of physiological components such as neurotransmitters, neurotrophic factors, receptors, cytokines, and ion-binding proteins in the body. For example, excessive fat intake can lead to depression, with possible mechanisms including inflammation, increased oxidative stress, reduced synaptic plasticity, and decreased expression of 5-Hydroxytryptamine (5-HT), Brain Derived Neurotrophic Factor (BDNF), Postsynaptic density protein 95(PSD-95), etc. Supplementing mineral elements, such as selenium, zinc, magnesium, or lithium as a psychotropic medication is mostly used as an auxiliary method to improve depression with other antidepressants. In general, appropriate nutritional elements are essential to treat depression and prevent the risk of depression.

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“…In addition to the synthetic agonists of GPBAR1, some natural agonists of GPBAR1 could also improve the cognitive function and alleviate depression. Working memory losses after consuming a high-fat diet and being inactive were avoided by using olive leaf extract, which contains oleanolic acid, a powerful GPBAR1 agonist [ 147 ]. TUDCA, a taurine conjugate of UDCA, together with GPBAR1/TGR5-boosted cAMP levels in microglia that triggered anti-inflammatory markers while reducing the pro-inflammatory ones [ 208 ].…”

Section: Bile Acid Signaling In Brain Diseasementioning

confidence: 99%

Linking Nonalcoholic Fatty Liver Disease and Brain Disease: Focusing on Bile Acid Signaling

Ren

Li²,

Ma³

et al. 2022

IJMS

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A metabolic illness known as non-alcoholic fatty liver disease (NAFLD), affects more than one-quarter of the world’s population. Bile acids (BAs), as detergents involved in lipid digestion, show an abnormal metabolism in patients with NAFLD. However, BAs can affect other organs as well, such as the brain, where it has a neuroprotective effect. According to a series of studies, brain disorders may be extrahepatic manifestations of NAFLD, such as depression, changes to the cerebrovascular system, and worsening cognitive ability. Consequently, we propose that NAFLD affects the development of brain disease, through the bile acid signaling pathway. Through direct or indirect channels, BAs can send messages to the brain. Some BAs may operate directly on the central Farnesoid X receptor (FXR) and the G protein bile acid-activated receptor 1 (GPBAR1) by overcoming the blood–brain barrier (BBB). Furthermore, glucagon-like peptide-1 (GLP-1) and the fibroblast growth factor (FGF) 19 are released from the intestine FXR and GPBAR1 receptors, upon activation, both of which send signals to the brain. Inflammatory, systemic metabolic disorders in the liver and brain are regulated by the bile acid-activated receptors FXR and GPBAR1, which are potential therapeutic targets. From a bile acid viewpoint, we examine the bile acid signaling changes in NAFLD and brain disease. We also recommend the development of dual GPBAR1/FXR ligands to reduce side effects and manage NAFLD and brain disease efficiently.

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Olive leaf extract prevents obesity, cognitive decline, and depression and improves exercise capacity in mice

Cited by 15 publications

References 59 publications

Exercise-Induced Lactate Release Mediates Mitochondrial Biogenesis in the Hippocampus of Mice via Monocarboxylate Transporters

Exercise-Induced Lactate Release Mediates Mitochondrial Biogenesis in the Hippocampus of Mice via Monocarboxylate Transporters

Appropriate Macronutrients or Mineral Elements Are Beneficial to Improve Depression and Reduce the Risk of Depression

Linking Nonalcoholic Fatty Liver Disease and Brain Disease: Focusing on Bile Acid Signaling

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