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High-Fat Diet, Obesity and Related Inflammation

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

Deadline for manuscript submissions: closed (5 May 2024) | Viewed by 10360

Special Issue Editor


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Guest Editor
Graduate School of Medicine, Nagoya University, Nagoya, Japan
Interests: diabetes; obesity; metabolic disease

Special Issue Information

Dear Colleagues,

Obesity is characterized by increased storage of body fat resulting from an imbalance between energy intake and energy expenditure, and it is well known that a high calorie diet is one of the main causes of obesity. Diet-induced obesity is associated with inflammation not only in the peripheral tissues but also in the brain, by which energy balance is primarily regulated. Energy balance is regulated by not only the homeostatic system, but also the reward system in the brain. It has been previously reported that a high-fat diet (HFD) causes inflammation in various places in the brain. The inflammation induced by HFD has been well studied in the arcuate nucleus region in the hypothalamus that regulates the homeostatic system, and it has been reported that inflammation occurs through the activation of both microglia and astrocytes, a state called gliosis. In addition, several lines of evidence indicate that inflammation occurs in reward-related brain regions by HFD. However, the detailed molecular mechanisms of the pathology underlying the dysregulation of the homeostatic and reward system caused by HFD-induced inflammation with gliosis remain unclear. Therefore, this Special Issue solicits submissions of original research on high-fat diets, obesity, and related inflammation, with a particular focus on the central nervous system.

Dr. Ryoichi Banno
Guest Editor

Manuscript Submission Information

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Keywords

  • high-fat diets
  • obesity
  • diet-induced inflammation
  • microglia
  • astrocytes
  • homeostatic system
  • reward system
  • hypothalamus
  • ventral tegmental area
  • striatum

Published Papers (4 papers)

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Research

17 pages, 6613 KiB  
Article
Effects of Gestational and Lactational Lead Exposure and High Fat Diet Feeding on Cerebellar Development of Postnatal Rat Offspring
by Jin Seok Seo, Shin Hyo Lee, Hyung-Sun Won, Miyoung Yang, Sang-Seop Nahm and Sung Min Nam
Nutrients 2023, 15(20), 4325; https://doi.org/10.3390/nu15204325 - 10 Oct 2023
Viewed by 1203
Abstract
Obesity and heavy metals, such as lead (Pb), are detrimental to the adult brain because they impair cognitive function and structural plasticity. However, the effects of co-administration of Pb and a high-fat diet (HFD) on the developing cerebellum is not clearly elucidated. We [...] Read more.
Obesity and heavy metals, such as lead (Pb), are detrimental to the adult brain because they impair cognitive function and structural plasticity. However, the effects of co-administration of Pb and a high-fat diet (HFD) on the developing cerebellum is not clearly elucidated. We investigated the effects of Pb exposure (0.3% lead acetate) on developing cerebellum in the pups of an HFD-fed obese rat model. One week before mating, we fed a chow diet (CD) or HFD to the rats for one week and additionally administered Pb to HFD-fed female SD rats. Thereafter, treatment with Pb and a HFD was continued during the gestational and lactational periods. On postnatal day 21, the pups were euthanized to sample the brain tissue and blood for further analysis. Blood Pb levels were significantly higher in HFD-fed rats than in CD-fed rats. Histologically, the prominent degeneration of Purkinje cells was induced by the co-administration of Pb and HFD. The calbindin-28Kd-, GAD67-, NMDAR1-, and PSD95-immunopositive Purkinje cells and inhibitory synapse-forming pinceau structures were significantly decreased following Pb and HFD co-administration. MBP-immunoreactive myelinated axonal fibers were also impaired by HFD but were significantly damaged by the co-administration of HFD and Pb. Oxidative stress-related Nrf2–HO1 signaling was activated by HFD feeding, and Pb exposure further aggravated oxidative stress, as demonstrated by the consumption of endogenous anti-oxidant in HFD–Pb rats. The pro-inflammatory response was also increased by the co-administration of HFD and Pb in the cerebellum of the rat offspring. The present results suggest that HFD and Pb treatment during the gestational and lactational periods are harmful to cerebellar development. Full article
(This article belongs to the Special Issue High-Fat Diet, Obesity and Related Inflammation)
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21 pages, 4361 KiB  
Article
Effects of High-Fat and High-Fat High-Sugar Diets in the Anxiety, Learning and Memory, and in the Hippocampus Neurogenesis and Neuroinflammation of Aged Rats
by Bárbara Mota, Miguel Ramos, Sandra I. Marques, Ana Silva, Pedro A. Pereira, M. Dulce Madeira, Nuno Mateus and Armando Cardoso
Nutrients 2023, 15(6), 1370; https://doi.org/10.3390/nu15061370 - 11 Mar 2023
Cited by 5 | Viewed by 3782
Abstract
High-caloric diets induce several deleterious alterations in the human body, including the brain. However, information on the effects of these diets on the elderly brain is scarce. Therefore, we studied the effects of 2 months of treatment with high-fat (HF) and high-fat-high-sugar (HFHS) [...] Read more.
High-caloric diets induce several deleterious alterations in the human body, including the brain. However, information on the effects of these diets on the elderly brain is scarce. Therefore, we studied the effects of 2 months of treatment with high-fat (HF) and high-fat-high-sugar (HFHS) diets on aged male Wistar rats at 18 months. Anxiety levels were analyzed using the open-field and plus-maze tests, while learning and memory processes were analyzed using the Morris water maze test. We also analyzed neurogenesis using doublecortin (DCX) and neuroinflammation using glial fibrillary acidic protein (GFAP). In aged rats, the HFHS diet impaired spatial learning, memory, and working memory and increased anxiety levels, associated with a reduction in the number of DCX cells and an increase in GFAP cells in the hippocampus. In contrast, the effects of the HF diet were lighter, impairing spatial memory and working memory, and associated with a reduction in DCX cells in the hippocampus. Thus, our results suggest that aged rats are highly susceptible to high-caloric diets, even if they only started in the elderly, with an impact on cognition and emotions. Furthermore, diets rich in saturated fats and sugar are more detrimental to aged rats than high-fat diets are. Full article
(This article belongs to the Special Issue High-Fat Diet, Obesity and Related Inflammation)
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12 pages, 2899 KiB  
Article
Inflammation in VTA Caused by HFD Induces Activation of Dopaminergic Neurons Accompanied by Binge-like Eating
by Runan Sun, Mariko Sugiyama, Sixian Wang, Mitsuhiro Kuno, Tomoyuki Sasaki, Tomonori Hirose, Takashi Miyata, Tomoko Kobayashi, Taku Tsunekawa, Takeshi Onoue, Yoshinori Yasuda, Hiroshi Takagi, Daisuke Hagiwara, Shintaro Iwama, Hidetaka Suga and Hiroshi Arima
Nutrients 2022, 14(18), 3835; https://doi.org/10.3390/nu14183835 - 16 Sep 2022
Cited by 5 | Viewed by 2082
Abstract
Binge eating is a characteristic symptom observed in obese individuals that is related to dysfunction of dopaminergic neurons (DNs). Intermittent administration of a high-fat diet (HFD) is reported to induce binge-like eating, but the underlying mechanisms remain unclear. We generated dopaminergic neuron specific [...] Read more.
Binge eating is a characteristic symptom observed in obese individuals that is related to dysfunction of dopaminergic neurons (DNs). Intermittent administration of a high-fat diet (HFD) is reported to induce binge-like eating, but the underlying mechanisms remain unclear. We generated dopaminergic neuron specific IKKβ deficient mice (KO) to examine the effects of inflammation in DNs on binge-like eating under inflammatory conditions associated with HFD. After administration of HFD for 4 weeks, mice were fasted for 24 h, and then the consumption of HFD was measured for 2 h. We also evaluated that the mRNA expressions of inflammatory cytokines, glial markers, and dopamine signaling-related genes in the ventral tegmental area (VTA) and striatum. Moreover, insulin was administered intraventricularly to assess downstream signaling. The consumption of HFD was significantly reduced, and the phosphorylation of AKT in the VTA was significantly increased in female KO compared to wild-type (WT) mice. Analyses of mRNA expressions revealed that DNs activity and inflammation in the VTA were significantly decreased in female KO mice. Thus, our data suggest that HFD-induced inflammation with glial cell activation in the VTA affects DNs function and causes abnormal eating behaviors accompanied by insulin resistance in the VTA of female mice. Full article
(This article belongs to the Special Issue High-Fat Diet, Obesity and Related Inflammation)
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15 pages, 9321 KiB  
Article
Inonotus hispidus Protects against Hyperlipidemia by Inhibiting Oxidative Stress and Inflammation through Nrf2/NF-κB Signaling in High Fat Diet Fed Mice
by Yongfeng Zhang, Jie Hao, Zijian Liu, Zhige Li, Lirong Teng and Di Wang
Nutrients 2022, 14(17), 3477; https://doi.org/10.3390/nu14173477 - 24 Aug 2022
Cited by 14 | Viewed by 2364
Abstract
Obesity is frequently associated with dysregulated lipid metabolism and lipotoxicity. Inonotus hispidus (Bull.: Fr.) P. Karst (IH) is an edible and medicinal parasitic mushroom. In this study, after a systematic analysis of its nutritional ingredients, the regulatory effects of IH on lipid metabolism [...] Read more.
Obesity is frequently associated with dysregulated lipid metabolism and lipotoxicity. Inonotus hispidus (Bull.: Fr.) P. Karst (IH) is an edible and medicinal parasitic mushroom. In this study, after a systematic analysis of its nutritional ingredients, the regulatory effects of IH on lipid metabolism were investigated in mice fed a high-fat diet (HFD). In HFD-fed mice, IH reversed the pathological state of the liver and the three types of fat and significantly decreased the levels of low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), triglycerides (TG), and leptin (LEP) and increased the level of high-density liptein cholesterol (HDL-C) in serum. Meanwhile, IH ameliorated liver damage by reducing alanine aminotransferase (ALT), aspartate aminotransferase (AST), interleukin (IL)-1β, IL-6, tumor necrosis factor-alpha (TNF-α), and plasminogen activator inhibitor-1 (PAI-1) levels in the liver and serum. Compared with HFD-fed mice, IH significantly modulated the gut microbiota, changed the relative abundances of microflora at different taxonomic levels, and regulated lipid levels. The results showed that 30 differential lipids were found. Results from Western blotting confirmed that IH regulated the nuclear factor erythroid-2 related factor 2 (Nrf2)/nuclear factor-kappa B (NF-κB) signaling pathway and oxidative stress. This study aimed to provide experimental evidence for the applicability of IH in obesity treatment. Full article
(This article belongs to the Special Issue High-Fat Diet, Obesity and Related Inflammation)
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