Short-term high-fat feeding exacerbates degeneration in retinitis pigmentosa by promoting retinal oxidative stress and inflammation

2021 ◽  
Vol 118 (43) ◽  
pp. e2100566118
Author(s):  
Oksana Kutsyr ◽  
Agustina Noailles ◽  
Natalia Martínez-Gil ◽  
Lucía Maestre-Carballa ◽  
Manuel Martinez-Garcia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Retinitis Pigmentosa ◽  
Retinal Degeneration ◽  
Gut Microbiome ◽  
Cell Activation ◽  
High Fat ◽  
Short Term ◽  
Oxidative Markers ◽  
Degenerative Disorders ◽  
Inflammatory State

A high-fat diet (HFD) can induce hyperglycemia and metabolic syndromes that, in turn, can trigger visual impairment. To evaluate the acute effects of HFD feeding on retinal degeneration, we assessed retinal function and morphology, inflammatory state, oxidative stress, and gut microbiome in dystrophic retinal degeneration 10 (rd10) mice, a model of retinitis pigmentosa, fed an HFD for 2 to 3 wk. Short-term HFD feeding impaired retinal responsiveness and visual acuity and enhanced photoreceptor degeneration, microglial cell activation, and Müller cell gliosis. HFD consumption also triggered the expression of inflammatory and oxidative markers in rd10 retinas. Finally, an HFD caused gut microbiome dysbiosis, increasing the abundance of potentially proinflammatory bacteria. Thus, HFD feeding drives the pathological processes of retinal degeneration by promoting oxidative stress and activating inflammatory-related pathways. Our findings suggest that consumption of an HFD could accelerate the progression of the disease in patients with retinal degenerative disorders.

scholarly journals High‐fat consumption alters the gut microbiome in retinitis pigmentosa mice and accelerates retinal degeneration

2022 ◽  
Vol 100 (S267) ◽  
Author(s):  
Oksana Kutsyr ◽  
Agustina Noailles ◽  
Natalia Martínez‐Gil ◽  
Lucía Maestre‐Carballa ◽  
Manuel Martínez‐García ◽  
...  
Keyword(s):  
Retinitis Pigmentosa ◽  
Retinal Degeneration ◽  
Gut Microbiome ◽  
High Fat ◽  
Fat Consumption

Kupffer cell activation is a causal factor for hepatic insulin resistance

2010 ◽  
Vol 298 (1) ◽  
pp. G107-G116 ◽  
Author(s):  
Nicolas Lanthier ◽  
Olivier Molendi-Coste ◽  
Yves Horsmans ◽  
Nico van Rooijen ◽  
Patrice D. Cani ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Kupffer Cell ◽  
High Fat Diet ◽  
Cell Activation ◽  
Hepatic Insulin Resistance ◽  
High Fat ◽  
Short Term ◽  
Adipose Tissue Macrophages ◽  
Diet Model

Recruited adipose tissue macrophages contribute to chronic and low-grade inflammation causing insulin resistance in obesity. Similarly, we hypothesized here that Kupffer cells, the hepatic resident macrophages, play a pathogenic role in hepatic insulin resistance induced by a high-fat diet. Mice were fed a normal diet or high-fat diet for 3 days. Kupffer cell activation was evaluated by immunohistochemistry and quantitative RT-PCR. Insulin sensitivity was assessed in vivo by hyperinsulinemic-euglycemic clamp and insulin-activated signaling was investigated by Western blot. Liposome-encapsulated clodronate was injected intravenously to deplete macrophages prior to a short-term exposure to high-fat diet. Here, we characterized a short-term high-fat diet model in mice and demonstrated early hepatic insulin resistance and steatosis concurrent with Kupffer cell activation. We demonstrated that selective Kupffer cell depletion obtained by intravenous clodronate, without affecting adipose tissue macrophages, was sufficient to enhance insulin-dependent insulin signaling and significantly improve hepatic insulin sensitivity in vivo in this short-term high-fat diet model. Our study clearly shows that hepatic macrophage response participates to the onset of high-fat diet-induced hepatic insulin resistance and may therefore represent an attractive target for prevention and treatment of diet- and obesity-induced insulin resistance.

scholarly journals (-)-Epicatechin Mitigates High Fat Diet-induced Inflammation in the Hippocampus and Altered Recognition Memory in Mice

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 411-411
Author(s):  
Jiye Kang ◽  
Ziwei Wang ◽  
Patricia Oteiza
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Object Recognition ◽  
Recognition Memory ◽  
High Fat Diet ◽  
High Fat ◽  
Short Term ◽  
Dietary Treatments ◽  
Metabolic Endotoxemia ◽  
And Oxidative Stress

Abstract Objectives This project investigated the capacity of dietary (-)-epicatechin (EC) to mitigate hippocampal inflammation and impaired memory in high fat diet (HFD)-fed mice. Methods Healthy 6 weeks old male C57BL/6J mice (10 mice/group) were fed for 13 weeks either: a control diet (10% total calories from fat), a high fat diet (60% total calories from lard fat), or the control and high fat diets supplemented with 20 mg EC/kg body weight. Between weeks 10 and 12 of the dietary intervention, object recognition memory was evaluated by the novel object recognition task and short-term spatial memory by the object location memory task, and the Morris Water Maze. After 13 weeks on the dietary treatments, mice were euthanized, and brain tissues and blood were collected. Hippocampus was isolated, flash-frozen in liquid nitrogen, and stored at −80°C. Metabolic endotoxemia was assessed by measuring plasma lipopolysaccharide (LPS) levels. Gene expressions related to inflammation (Toll-like receptor 4 (TLR4) and tumor necrosis factor-α (TNF-α)), activation of microglia (ionized calcium-binding adapter molecule 1 (Iba-1)), and oxidative stress (NADPH oxidase 4 (NOX4)) were analyzed in the hippocampus with RT-qPCR. Results After 13 weeks on the dietary treatments, HFD-fed mice developed obesity, endotoxemia, and showed increased parameters of hippocampal inflammation, i.e., high mRNA levels of TLR4, Iba-1, and NOX4. While not affecting body weight gain, EC supplementation prevented all other HFD-induced changes. Impaired recognition memory was observed in HFD-fed mice, which was prevented by EC supplementation. Neither HFD consumption nor EC supplementation affected mouse spatial memory. Conclusions EC supplementation prevented short-term recognition memory in HFD-induced obese mice, which could be in part due to the capacity of EC to mitigate metabolic endotoxemia and associated hippocampal inflammation and oxidative stress. Funding Sources HA Jastro Shields Award.

Abstract P481: Short-term Synbiotic, B420 And Oligofructose, Treatment Reverse High-fat-diet Related Pathologies In Ischemic Reperfusion Mouse Models

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Christina H Hoyer-Kimura ◽  
Christine Behm ◽  
Joshua P Fricks ◽  
Frank Duca ◽  
John P Konhilas
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Infarct Size ◽  
Gut Microbiome ◽  
High Fat Diet ◽  
Male Mice ◽  
High Fat ◽  
Short Term ◽  
Short Term Treatment ◽  
Ischemic Reperfusion

The gut microbiome impacts metabolic homeostasis, and several inflammatory pathologies including obesity, glucose intolerance, and worsened cardiovascular disease outcomes are associated with an altered gut microbiome. We have previously demonstrated Bifidobacterium animalis lactis 420 ([B420], a probiotic) attenuates myocardial infarct injury in mice following ischemic reperfusion (IR) injury. Further, Oligofructose ([OFS], a prebiotic) improves glucose tolerance, and reduces weight gain in high-fat-diet (HFD) mice. However, the combined ability of B420 and OFS (a synbiotic) on cardiovascular and metabolic disease is unknown. We hypothesized that short-term (2 weeks) synbiotic treatment improves adiposity and glucose tolerance and reduces IR infarct size in HFD fed male mice more than prebiotic or probiotic treatments alone. Adult male mice were fed HFD (45% fat) for 2 weeks and were then treated with OFS (10microliters/gram weight, 200miligram OFS/ 300microliters saline), B420 (10microliters/gram weight, 10 9 CFU/ 300microliters saline), or B420+OFS (synbiotic treatment) via daily gavage for 2 weeks. Following treatment mice underwent an IR protocol, (45-minute ligation followed by reperfusion). Oral glucose tolerance tests were conducted prior to and after treatment to determine blood glucose. Fasted mice were gavaged with glucose (2.5g/kg glucose) and blood glucose was measured over 120 minutes. Body weight, and kcal intake were measured weekly. Upon sacrifice epididymal fat mas was weighed to determine adiposity. Data were analyzed by one-way ANOVA or T-test. We found that short-term synbiotic treatment with B420+OFS during HFD-feeding reduced adiposity and improved glucose tolerance, while probiotic or prebiotic treatment alone had no effect. However, short-term treatment, including synbiotic, did not significantly reduce heart infarct size as previously demonstrated with longer treatment periods. Taken together, these results suggest that synbiotic treatment improves metabolic impairments more rapidly than B420 or OFS alone, and precedes improvements in infarct size.

scholarly journals Induced Short-Term Hearing Loss due to Stimulation of Age-Related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection

2020 ◽  
Vol 21 (19) ◽  
pp. 7068
Author(s):  
Dong Jun Park ◽  
Sunmok Ha ◽  
Jin Sil Choi ◽  
Su Hoon Lee ◽  
Jeong-Eun Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
High Fat Diet ◽  
Intermittent Hypoxia ◽  
Environmental Changes ◽  
Cellular Aging ◽  
High Fat ◽  
Short Term ◽  
Related Factors ◽  
Age Related

Age-related hearing loss (ARHL) is the most common sensory disorder among the elderly, associated with aging and auditory hair cell death due to oxidative-stress-induced mitochondrial dysfunction. Although transgenic mice and long-term aging induction cultures have been used to study ARHL, there are currently no ARHL animal models that can be stimulated by intermittent environmental changes. In this study, an ARHL animal model was established by inducing continuous oxidative stress to promote short-term aging of cells, determined on the basis of expression of hearing-loss-induced phenotypes and aging-related factors. The incidence of hearing loss was significantly higher in dual- and triple-exposure conditions than in intermittent hypoxic conditions, high-fat diet (HFD), or d-galactose injection alone. Continuous oxidative stress and HFD accelerated cellular aging. An increase in Ucp2, usually expressed during mitochondrial dysfunction, was observed. Expression of Cdh23, Slc26a4, Kcnq4, Myo7a, and Myo6, which are ARHL-related factors, were modified by oxidative stress in the cells of the hearing organ. We found that intermittent hypoxia, HFD, and galactose injection accelerated cellular aging in the short term. Thus, we anticipate that the development of this hearing loss animal model, which reflects the effects of intermittent environmental changes, will benefit future research on ARHL.

scholarly journals Induced Short-term Hearing Loss due to Stimulation of Age-related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection

2020 ◽  
Author(s):  
Dong Jun Park ◽  
Sunmok Ha ◽  
Jin Sil Choi ◽  
Su Hoon Lee ◽  
Jeong-Eun Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Animal Model ◽  
Hearing Loss ◽  
Mitochondrial Dysfunction ◽  
High Fat Diet ◽  
Cellular Aging ◽  
High Fat ◽  
Short Term ◽  
Related Factors ◽  
Age Related

Age-related hearing loss (ARHL) is the most common sensory disorder in the elderly. It is associated with aging and hair cell death due to oxidative stress-induced mitochondrial dysfunction. Although transgenic mice and long-term cultures for induction of aging have been used to study ARHL, there are presently no ARHL animal models stimulated by intermittent environmental change for aging. In this study, an ARHL animal model was established by inducing continuous oxidative stress to promote short-term aging of cells, determined based on the expression of the hearing loss-induced phenotype and aging related factors in the short term. The incidence of hearing loss was significantly different among the groups subjected to intermittent hypoxic environment, high-fat diet (HFD), and injection with D-galactose. Continuous oxidative stress and HFD were factors that accelerated cellular aging. Increase in UCP2 affected oxidative stress and mitochondrial dysfunction. CDH23, SLC26A4, KCNQ4, Myo7a, and Myo6, which are ARHL-related factors, were modified by oxidative stress in cells of the hearing organ. We found that intermittent hypoxic, HFD, and galactose injection accelerated cellular aging in the short term. Thus, we anticipate that the development of this hearing loss animal model, which reflects intermittent environmental changes, will benefit future research on ARHL.

Impairment of Long-term Memory by a Short-term High-fat Diet via Hippocampal Oxidative Stress and Alterations in Synaptic Plasticity

Neuroscience ◽  
2020 ◽  
Vol 424 ◽  
pp. 24-33 ◽  
Author(s):  
Zhengjun Wang ◽  
Qian Ge ◽  
Yuwei Wu ◽  
Jinming Zhang ◽  
Qiaofen Gu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Synaptic Plasticity ◽  
High Fat Diet ◽  
Long Term Memory ◽  
High Fat ◽  
Short Term ◽  
Term Memory
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