Abstract
This study was conducted to assess the protective effect of extract of match (EM) on high-fat diet- (HFD-) induced cognitive deficits in male C57BL/6 mice. It was found that EM improved glucose tolerance status by measuring OGTT and IPGTT with HFD-induced mice. EM protected behavioral and memory dysfunction in Y-maze, passive avoidance, and Morris water maze tests. Consumption of EM reduced fat mass, dyslipidemia, and inflammation in adipose tissue. Also, EM ameliorated hepatic and cerebral antioxidant systems. EM improved the cerebral cholinergic system by regulating ACh contents and expression of AChE and ChAT. Also, EM restored mitochondrial function in liver and brain tissue. EM attenuated hepatic inflammatory effect, lipid synthesis, and cholesterol metabolism by regulating the protein expression of TNF-α, TNFR1, p-IRS-1, p-JNK, IL-1β, iNOS, COX-2, HMGCR, PPARγ, and FAS. Finally, EM regulated cognitive function and neuroinflammation in the whole brain, hippocampus, and cerebral cortex by regulating the protein expression of p-JNK, p-Akt, p-tau, Aβ, BDNF, IDE, COX-2, and IL-1β. These findings suggest that EM might be a potential source of functional food to improve metabolic disorder-associated cognitive dysfunction.
Highlights
Diabetes is one of the metabolic diseases caused by the consumption of a high-fat diet (HFD) and causes metabolic disorders such as dyslipidemia, insulin resistance, hepatic steatosis, and nonalcoholic fatty liver disease [1]
Hydroxylamine·hydrochloride, phenylmethane sulfonylfluoride, thiobarbituric acid (TBA), metaphosphoric acid, o-phthaldialdehyde, bovine serum albumin (BSA), HEPES, digitonin, 2′,7′-dichlorofluorescein diacetate (DCF-DA), tetrachloro-1,1,3,3-tetraethylbenzimidazolylcarbo-cyanine iodide (JC-1), polyvinylidene difluoride, iron (III) chloride hexahydrate, protease inhibitor (PI), and polyvinylidene difluoride (PVDF) membrane were purchased from Millipore (Billerica, MA, USA)
This study confirmed that matcha can effectively protect against insulin resistance and cognitive impairment caused by hepatic and cerebral inflammatory responses in high-fat diet- (HFD-)induced mice
Summary
Diabetes is one of the metabolic diseases caused by the consumption of a high-fat diet (HFD) and causes metabolic disorders such as dyslipidemia, insulin resistance, hepatic steatosis, and nonalcoholic fatty liver disease [1]. The liver plays an important role in diabetes-related insulin resistance and hepatic glucose production by regulating gluconeogenesis and glycogenolysis by activating immune cells secreting inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin 1 beta (IL-1β) [3, 4]. Brain tissue is known to be a tissue that is susceptible to damage due to the inflammatory reaction caused by HFD [7]. Cognitive dysfunction induced by inflammation is associated with reactive oxygen species (ROS) production and mitochondrial damage in brain tissue, and impaired mitochondrial dysfunction continuously causes insulin resistance in cerebral neuronal cells [4, 8]. Insulin resistance increases the problems associated with diabetic cognitive dysfunction, which leads to diseases such as Alzheimer’s disease (AD) [9]
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