scholarly journals Young APPKI NL-G-F/NL-G-F mice display high-fat diet-induced metabolic disturbances and specific disorders associated with brain energy homeostasis.

2021 ◽  
Author(s):  
Wei Wang ◽  
Daisuke Tanokashira ◽  
Megumi Maruyama ◽  
Chiemi Kuroiwa ◽  
Takashi Saito ◽  
...  
Keyword(s):  
Mouse Models ◽  
High Fat Diet ◽  
Early Life ◽  
Energy Homeostasis ◽  
Normal Diet ◽  
Aging Effects ◽  
High Fat ◽  
Metabolic Disturbances ◽  
Increased Risk ◽  
Brain Energy

Aim: Type 2 diabetes mellitus (T2DM) is an increased risk factor for Alzheimer's disease (AD); however, the relationship between the two conditions is controversial. High-fat diet (HFD) causes cognitive impairment with/without Aβ accumulation in middle-aged or aged transgenic (Tg) and knock-in (KI) AD mouse models, except for metabolic disorders, which commonly occur in all mice types. Alternatively, whether HFD in early life impacts energy metabolism and neurological phenotypes in young AD mouse models remains unknown. In the present study, we examined the effects of HFD on young APPKI NL-G-F/NL-G-F mice, one of the novel knock-in (KI)-AD mouse models. Methods: The mice were categorized by diet into two experimental groups, normal diet (ND) and HFD. Four-week-old WT and APPKI NL-G-F/NL-G-F mice were fed ND or HFD for nine weeks. Both types of mice on ND and HFD were examined during young adulthood. Results: HFD causes T2DM-related metabolic disturbances in young WT and APPKI NL-G-F/NL-G-F mice and specific impairment of brain energy homeostasis only in young APPKI NL-G-F/NL-G-F mice. However, HFD-induced metabolic dysfunctions had no impact on behaviors, Aβ levels, and specific IRS1 modifications in both young APPKI NL-G-F/NL-G-F mice and young WT mice. Conclusion: HFD in early life is effective in causing metabolic disturbances in young WT and APPKI NL-G-F/NL-G-F mice but is ineffective in inducing neurological disorders in young mice, which suggests that the aging effects along with long-term HFD cause neurological alterations.

scholarly journals Maternal separation-induced increases in vascular stiffness are independent of circulating angiotensinogen levels

2020 ◽  
Vol 129 (1) ◽  
pp. 58-65
Author(s):  
Timothy M. Mahanes ◽  
Margaret O. Murphy ◽  
An Ouyang ◽  
Frederique B. Yiannikouris ◽  
Bradley S. Fleenor ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Life Stress ◽  
Early Life ◽  
Maternal Separation ◽  
Early Life Stress ◽  
Normal Diet ◽  
Vascular Stiffness ◽  
High Fat ◽  
Vascular Contractility ◽  
Circulating Levels

This study demonstrates that there was no correlation between circulating levels of angiotensinogen (AGT) and the development of vascular stiffness in rats exposed to early-life stress and fed a normal diet. This study also shows that early-life stress-induced hypersensitive vascular contractility to angiotensin II in rats fed a high-fat diet is independent of circulating levels of AGT and occurs without further progression of vascular stiffness. Our data show that early-life stress primes the adipose tissue to secrete AGT in a sex- and species-independent fashion.

scholarly journals Estradiol and high fat diet associate with changes in gut microbiota in female ob/ob mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kalpana D. Acharya ◽  
Xing Gao ◽  
Elizabeth P. Bless ◽  
Jun Chen ◽  
Marc J. Tetel
Keyword(s):  
Weight Gain ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Energy Homeostasis ◽  
Low Grade ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Increased Risk ◽  
17Β Estradiol ◽  
Low Grade Inflammation

AbstractEstrogens protect against diet-induced obesity in women and female rodents. For example, a lack of estrogens in postmenopausal women is associated with an increased risk of weight gain, cardiovascular diseases, low-grade inflammation, and cancer. Estrogens act with leptin to regulate energy homeostasis in females. Leptin-deficient mice (ob/ob) exhibit morbid obesity and insulin resistance. The gut microbiome is also critical in regulating metabolism. The present study investigates whether estrogens and leptin modulate gut microbiota in ovariectomized ob/ob (obese) or heterozygote (lean) mice fed high-fat diet (HFD) that received either 17β-Estradiol (E2) or vehicle implants. E2 attenuated weight gain in both genotypes. Moreover, both obesity (ob/ob mice) and E2 were associated with reduced gut microbial diversity. ob/ob mice exhibited lower species richness than control mice, while E2-treated mice had reduced evenness compared with vehicle mice. Regarding taxa, E2 was associated with an increased abundance of the S24-7 family, while leptin was associated with increases in Coriobacteriaceae, Clostridium and Lactobacillus. Some taxa were affected by both E2 and leptin, suggesting these hormones alter gut microbiota of HFD-fed female mice. Understanding the role of E2 and leptin in regulating gut microbiota will provide important insights into hormone-dependent metabolic disorders in women.

scholarly journals Cardiometabolic Syndrome: An Update on Available Mouse Models

2020 ◽  
Author(s):  
Styliani Vakrou ◽  
Dimitra Aravani ◽  
Eva Kassi ◽  
Antonios Chatzigeorgiou
Keyword(s):  
Mouse Models ◽  
High Fat Diet ◽  
Animal Species ◽  
Genetic Manipulation ◽  
Genetically Engineered ◽  
High Fat ◽  
Cardiometabolic Syndrome ◽  
Global Epidemic ◽  
Genetically Engineered Mouse Models ◽  
Increased Risk

AbstractCardiometabolic syndrome (CMS), a disease entity characterized by abdominal obesity, insulin resistance (IR), hypertension, and hyperlipidemia, is a global epidemic with approximately 25% prevalence in adults globally. CMS is associated with increased risk for cardiovascular disease (CVD) and development of diabetes. Due to its multifactorial etiology, the development of several animal models to simulate CMS has contributed significantly to the elucidation of the disease pathophysiology and the design of therapies. In this review we aimed to present the most common mouse models used in the research of CMS. We found that CMS can be induced either by genetic manipulation, leading to dyslipidemia, lipodystrophy, obesity and IR, or obesity and hypertension, or by administration of specific diets and drugs. In the last decade, the ob/ob and db/db mice were the most common obesity and IR models, whereas Ldlr−/− and Apoe−/− were widely used to induce hyperlipidemia. These mice have been used either as a single transgenic or combined with a different background with or without diet treatment. High-fat diet with modifications is the preferred protocol, generally leading to increased body weight, hyperlipidemia, and IR. A plethora of genetically engineered mouse models, diets, drugs, or synthetic compounds that are available have advanced the understanding of CMS. However, each researcher should carefully select the most appropriate model and validate its consistency. It is important to consider the differences between strains of the same animal species, different animals, and most importantly differences to human when translating results.

scholarly journals Leptin Signaling Is Required for Leucine Deprivation-enhanced Energy Expenditure

2013 ◽  
Vol 289 (3) ◽  
pp. 1779-1787 ◽  
Author(s):  
Qian Zhang ◽  
Bin Liu ◽  
Ying Cheng ◽  
Qingshu Meng ◽  
Tingting Xia ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
High Fat Diet ◽  
Energy Homeostasis ◽  
Leptin Receptor ◽  
Normal Diet ◽  
Leptin Resistance ◽  
High Fat ◽  
Leptin Signaling ◽  
Fat Loss ◽  
Stimulation Of

Leptin signaling in the hypothalamus is crucial in energy homeostasis. We have previously shown that dietary deprivation of the essential amino acid leucine in mice stimulates fat loss by increasing energy expenditure. The involvement of leptin signaling in this regulation, however, has not been reported. Here, we show that leucine deprivation promotes leptin signaling in mice maintained on an otherwise normal diet and restores leptin responses in mice maintained on a high fat diet, a regimen known to induce leptin resistance. In addition, we found that leucine deprivation stimulated energy expenditure, and fat loss was largely blocked in db/db mice homozygous for a mutation in leptin receptor and a knock-in mouse line Y3F with abrogation of leptin receptor Tyr1138-mediated signal transducer and activator transcript 3 signaling. Overall, our studies describe a novel link between hypothalamic leptin signaling and stimulation of energy expenditure under leucine deprivation.

Abstract P181: Contrasting Effects of High Fat Diet and DOCA-salt on Primary Neuronal Cilia

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Jingwei Jiang ◽  
Kamal Rahmouni
Keyword(s):  
High Fat Diet ◽  
Energy Homeostasis ◽  
Cardiovascular Regulation ◽  
Brain Regions ◽  
Normal Diet ◽  
High Fat ◽  
Pronounced Difference ◽  
Software Analysis ◽  
Neuronal Cilia ◽  
The Brain

Virtually, every mammalian cell is equipped with an antenna like primary cilium, a cell surface protrusion that is thought to act as a sensory organelle. Many of the rare genetic disorders that cause shorter, absent or disrupted cilia are associated with obesity and cardiovascular dysfunction in humans and rodents, which suggest that cilia length contribute to energy balance and cardiovascular homeostasis. Here, we examined the length of the primary neuronal cilia in the brain nuclei that contribute to metabolic and cardiovascular regulation in high fat diet-induced obese (DIO) mice and DOCA-salt mice. Cilia length was examined by adenylate cyclase 3 (AC3) immunostaining, followed by confocal 3D reconstruction, and quantification by IMARIS imaging analysis software. Analysis of the cilia length and distribution showed reduced frequency of cilia that are over 10 μm in the brain of DIO mice compared to control mice fed normal diet fed mice (17.02±1.36% vs 23.78±1.15%, p=0.032). Interestingly, the most pronounced difference in cilia length was observed in the dorsomedial hypothalamus with the DIO mice displaying significantly shorter cilia (6.90±0.06 μm) relative to controls (7.32±0.14μm in controls, n=5/group p<0.05). Conversely, we found that average neuronal cilia length was elongated in 3-week DOCA-salt treated mice compared to sham group. The number of primary neuronal cilia that are over 10 μm was significantly increased in DOCA-salt mice by 8% (p=0.0114). On the other hand, the number of cilia that are 4-5 μm in length was significantly decreased in DOCA-salt mice compared to sham controls (11.73±1.70% vs 18.73±2.02%, p=0.0385). The supraoptic nucleus was the only nucleus that displayed difference in the length of cilia that are 5-10 μm in length (7.46±0.24 μm vs 6.76±0.15μm, n=5/group, p=0.0509). Our data demonstrate plasticity of neuronal cilia in response to high fat diet and DOCA-salt treatment in defined brain regions. Our results raise the possibility that primary neuronal cilia may function as part of environmental surveillance system in the brain that control energy homeostasis and cardiovascular function. Further analysis of the role of primary neuronal cilia in cardiovascular regulation is underway.

scholarly journals Exposure to maternal high-fat diet induces extensive changes in the brain of adult offspring

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Darren J. Fernandes ◽  
Shoshana Spring ◽  
Anna R. Roy ◽  
Lily R. Qiu ◽  
Yohan Yee ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Early Life ◽  
Brain Regions ◽  
Autism Spectrum ◽  
Long Term Effects ◽  
High Fat ◽  
Reward Seeking ◽  
Low Fat Diet ◽  
Increased Risk ◽  
Fat Diets

AbstractMaternal environmental exposures, such as high-fat diets, diabetes and obesity, can induce long-term effects in offspring. These effects include increased risk of neurodevelopmental disorders (NDDs) including autism spectrum disorder (ASD), depression and anxiety. The mechanisms underlying these late-life neurologic effects are unknown. In this article, we measured changes in the offspring brain and determined which brain regions are sensitive to maternal metabolic milieu and therefore may mediate NDD risk. We showed that mice exposed to a maternal high-fat diet display extensive brain changes in adulthood despite being switched to a low-fat diet at weaning. Brain regions impacted by early-life diet include the extended amygdalar system, which plays an important role in reward-seeking behaviour. Genes preferentially expressed in these regions have functions related to feeding behaviour, while also being implicated in human NDDs, such as autism. Our data demonstrated that exposure to maternal high-fat diet in early-life leads to brain alterations that persist into adulthood, even after dietary modifications.

scholarly journals Exposure to maternal high-fat diet induces extensive changes in the brain of adult offspring

2020 ◽  
Author(s):  
Darren J. Fernandes ◽  
Shoshana Spring ◽  
Anna R. Roy ◽  
Lily R. Qiu ◽  
Yohan Yee ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Early Life ◽  
Brain Regions ◽  
Autism Spectrum ◽  
Long Term Effects ◽  
High Fat ◽  
Reward Seeking ◽  
Low Fat Diet ◽  
Increased Risk ◽  
Fat Diets

AbstractMaternal environmental exposures, such as high-fat diets, diabetes and obesity, can induce long term effects in offspring. These effects include increased risk of neurodevelopmental disorders (NDDs) including autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), depression and anxiety. The mechanisms underlying these late-life neurologic effects are unknown. In this article, we measured changes in the offspring brain and determined which brain regions are sensitive to maternal metabolic milieu and therefore may mediate NDD risk. We showed that mice exposed to maternal high-fat diet display extensive brain changes in adulthood despite being switched to low-fat diet at weaning. Brain regions impacted by early-life diet include the extended amygdalar system, which plays an important role in reward-seeking behaviour. Genes preferentially expressed in these regions have functions related to feeding behavior, while also being implicated in human NDDs, such as autism. Our data demonstrated that exposure to maternal high-fat diet in early-life leads to brain alterations that persist into adulthood, even after dietary modifications.

Non-Fasting Factor VII Coagulant Activity (FVII:C) Increased by High-Fat Diet

1994 ◽  
Vol 71 (06) ◽  
pp. 755-758 ◽  
Author(s):  
E M Bladbjerg ◽  
P Marckmann ◽  
B Sandström ◽  
J Jespersen
Keyword(s):  
High Fat Diet ◽  
Fat Content ◽  
Factor Vii ◽  
Amidolytic Activity ◽  
High Fat ◽  
Low Fat Diet ◽  
Increased Risk ◽  
Coagulant Activity ◽  
High Fat Diets ◽  
Fat Diets

SummaryPreliminary observations have suggested that non-fasting factor VII coagulant activity (FVII:C) may be related to the dietary fat content. To confirm this, we performed a randomised cross-over study. Seventeen young volunteers were served 2 controlled isoenergetic diets differing in fat content (20% or 50% of energy). The 2 diets were served on 2 consecutive days. Blood samples were collected at 8.00 h, 16.30 h and 19.30 h, and analysed for triglycerides, FVII coagulant activity using human (FVII:C) or bovine thromboplastin (FVII:Bt), and FVII amidolytic activity (FVIPAm). The ratio FVII:Bt/FVII:Am (a measure of FVII activation) increased from fasting levels on both diets, but most markedly on the high-fat diet. In contrast, FVII: Am (a measure of FVII protein) tended to decrease from fasting levels on both diets. FVII:C rose from fasting levels on the high-fat diet, but not on the low-fat diet. The findings suggest that high-fat diets increase non-fasting FVII:C, and consequently may be associated with increased risk of thrombosis.

Effects of dietary n-3 PUFA levels in early life on susceptibility to high-fat-diet-induced metabolic syndrome in adult mice

2020 ◽  
pp. 108578
Author(s):  
Dan-Dan Wang ◽  
Fang Wu ◽  
Ling-Yu Zhang ◽  
Ying-Cai Zhao ◽  
Cheng-Cheng Wang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
High Fat Diet ◽  
Early Life ◽  
High Fat ◽  
Adult Mice
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