The Protective Effects of Acer okamotoanum and Isoquercitrin on Obesity and Amyloidosis in a Mouse Model

Obesity increases risk of Alzheimer’s Disease (AD). A high fat diet (HFD) can lead to amyloidosis and amyloid beta (Aβ) accumulation, which are hallmarks of AD. In this study, protective effects of the ethyl acetate fraction of Acer okamotoanum (EAO) and isoquercitrin were evaluated on obesity and amyloidosis in the HFD- and Aβ-induced mouse model. To induce obesity and AD by HFD and Aβ, mice were provided with HFD for 10 weeks and were intracerebroventricularly injected with Aβ25–35. For four weeks, 100 and 10 mg/kg/day of EAO and isoquercitrin, respectively, were administered orally. Administration of EAO and isoquercitrin significantly decreased body weight in HFD and Aβ-injected mice. Additionally, EAO- and isoquercitrin-administered groups attenuated abnormal adipokines release via a decrease in leptin and an increase in adiponectin levels compared with the control group. Furthermore, HFD and Aβ-injected mice had damaged liver tissues, but EAO- and isoquercitrin-administered groups attenuated liver damage. Moreover, administration of EAO and isoquercitrin groups down-regulated amyloidosis-related proteins in the brain such as β-secretase, presenilin (PS)-1 and PS-2 compared with HFD and Aβ-injected mice. This study indicated that EAO and isoquercitrin attenuated HFD and Aβ-induced obesity and amyloidosis, suggesting that they could be effective in preventing and treating both obesity and AD.

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Protective Effects of Polyphenol Enriched Complex Plants Extract on Metabolic Dysfunctions Associated with Obesity and Related Nonalcoholic Fatty Liver Diseases in High Fat Diet-Induced C57BL/6 Mice

Molecules ◽

10.3390/molecules26020302 ◽

2021 ◽

Vol 26 (2) ◽

pp. 302

Author(s):

Ahtesham Hussain ◽

Jin Sook Cho ◽

Jong-Seok Kim ◽

Young Ik Lee

Keyword(s):

Body Weight ◽

Blood Glucose ◽

Mouse Model ◽

High Fat Diet ◽

Liver Diseases ◽

Liver Weight ◽

Control Group ◽

High Fat ◽

Herbal Formulation ◽

Plants Extract

Background: Currently, obesity is a global health challenge due to its increasing prevalence and associated health risk. It is associated with various metabolic diseases, including diabetes, hypertension, cardiovascular disease, stroke, certain forms of cancer, and non-alcoholic liver diseases (NAFLD). Objective: The aim of this study to evaluate the effects of polyphenol enriched herbal complex (Rubus crataegifolius/ellagic acid, Crataegus pinnatifida Bunge/vitexin, chlorogenic acid, Cinnamomum cassiaa/cinnamic acid) on obesity and obesity induced NAFLD in the high-fat diet (HFD)-induced obese mouse model. Methods: Obesity was induced in male C57BL/6 mice using HFD. After 8 weeks, the mice were treated with HFD+ plants extract for 8 weeks. Body weight, food intake weekly, and blood sugar level were measured. After sacrifice, changes in the treated group’s liver weight, fat weight, serum biochemical parameters, hormone levels, and enzyme levels were measured. For histological analysis, tissues were stained with hematoxylin-eosin (H&E) and Oil Red-O. Results: Our results showed that the herbal complex ameliorated body weight and liver weight gain, and decreased total body fat in HFD-fed animals. Post prandial blood glucose (PBG) and fasting blood glucose (FBG) were lower in the herbal complex-treated group than in the HFD control group. Additionally, herbal formulation treatment significantly increased HDL levels in serum and decreased TC, TG, AST, ALT, deposition of fat droplets in the liver, and intima media thickness (IMT) in the aorta. Herbal complex increased serum adiponectin and decreased serum leptin. Herbal complex also increased carnitine palmityl transferase (CPT) activity and significantly decreased enzyme activity of beta-hydroxy beta methyl glutamyl-CoA (HMG-CoA) reductase, and fatty acid synthase (FAS). Conclusions: The results of this study demonstrated that the herbal complex is an effective herbal formulation in the attenuation of obesity and obesity-induced metabolic dysfunction including NAFLD in HFD-induced mouse model.

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Effect of Anthocyanin-Rich Tart Cherry Extract on Inflammatory Mediators and Adipokines Involved in Type 2 Diabetes in a High Fat Diet Induced Obesity Mouse Model

Nutrients ◽

10.3390/nu11091966 ◽

2019 ◽

Vol 11 (9) ◽

pp. 1966 ◽

Cited By ~ 8

Author(s):

Nemes ◽

Homoki ◽

Kiss ◽

Hegedűs ◽

Kovács ◽

...

Keyword(s):

Body Weight ◽

Glucose Tolerance ◽

Mouse Model ◽

Antioxidant Capacity ◽

Inflammatory Mediators ◽

High Fat Diet ◽

Control Group ◽

Tart Cherry ◽

High Fat ◽

Sod Activity

Male C57BL/6J mice were used to determine the possible therapeutic effects of our previously described tart cherry extract in a chronic obesity mouse model on metabolic parameters, glucose tolerance, inflammatory mediators, and antioxidant capacity. The control group received standard mouse chow, and the high fat control group was switched to a high fat diet and tap water supplemented with 5% sucrose. The high fat + anthocyanin group received the high fat and sucrose diet, but received the anthocyanin-rich tart cherry extract dissolved in their drinking water. After six weeks, an oral glucose tolerance test was performed, and the water-soluble antioxidant capacity (ACW), superoxide dismutase (SOD) activity, and the plasma levels of insulin, C-peptide, leptin, IL-6, MCP-1, adiponectin and resistin were measured. The high fat diet increased body weight, reduced glucose tolerance, and caused an elevation in leptin, IL-6, MCP-1, and resistin levels. Furthermore, antioxidant capacity was decreased with a significant elevation of SOD activity. Anthocyanin treatment failed to reverse the effects of the high fat diet on body weight and glucose tolerance, but significantly reduced the leptin and IL-6 levels. The tart cherry extract also made a significant enhancement in antioxidant capacity and SOD activity. Our results show that chronic anthocyanin intake has a potential to enhance redox status and alleviate inflammation associated with obesity.

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High-fat diet-induced obesity and impairment of brain neurotransmitter pool

Translational Neuroscience ◽

10.1515/tnsci-2020-0099 ◽

2020 ◽

Vol 11 (1) ◽

pp. 147-160

Author(s):

Ranyah Shaker M. Labban ◽

Hanan Alfawaz ◽

Ahmed T. Almnaizel ◽

Wail M. Hassan ◽

Ramesa Shafi Bhat ◽

...

Keyword(s):

Oxidative Stress ◽

Brain Tissue ◽

High Fat Diet ◽

Density Lipoprotein ◽

Obese Group ◽

Control Group ◽

High Fat ◽

Brain Neurotransmitter ◽

The Brain ◽

Lean Group

AbstractObesity and the brain are linked since the brain can control the weight of the body through its neurotransmitters. The aim of the present study was to investigate the effect of high-fat diet (HFD)-induced obesity on brain functioning through the measurement of brain glutamate, dopamine, and serotonin metabolic pools. In the present study, two groups of rats served as subjects. Group 1 was fed a normal diet and named as the lean group. Group 2 was fed an HFD for 4 weeks and named as the obese group. Markers of oxidative stress (malondialdehyde, glutathione, glutathione-s-transferase, and vitamin C), inflammatory cytokines (interleukin [IL]-6 and IL-12), and leptin along with a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein levels) were measured in the serum. Neurotransmitters dopamine, serotonin, and glutamate were measured in brain tissue. Fecal samples were collected for observing changes in gut flora. In brain tissue, significantly high levels of dopamine and glutamate as well as significantly low levels of serotonin were found in the obese group compared to those in the lean group (P > 0.001) and were discussed in relation to the biochemical profile in the serum. It was also noted that the HFD affected bacterial gut composition in comparison to the control group with gram-positive cocci dominance in the control group compared to obese. The results of the present study confirm that obesity is linked to inflammation, oxidative stress, dyslipidemic processes, and altered brain neurotransmitter levels that can cause obesity-related neuropsychiatric complications.

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Effect of selective expression of dominant-negative PPARγ in pro-opiomelanocortin neurons on the control of energy balance

Physiological Genomics ◽

10.1152/physiolgenomics.00032.2016 ◽

2016 ◽

Vol 48 (7) ◽

pp. 491-501 ◽

Cited By ~ 9

Author(s):

Madeliene Stump ◽

Deng-Fu Guo ◽

Ko-Ting Lu ◽

Masashi Mukohda ◽

Xuebo Liu ◽

...

Keyword(s):

Body Weight ◽

Weight Gain ◽

Energy Balance ◽

High Fat Diet ◽

Control Diet ◽

Cre Recombinase ◽

Dominant Negative ◽

High Fat ◽

Pparγ Agonist ◽

The Brain

Peroxisome proliferator-activated receptor-γ (PPARγ), a master regulator of adipogenesis, was recently shown to affect energy homeostasis through its actions in the brain. Deletion of PPARγ in mouse brain, and specifically in the pro-opiomelanocortin (POMC) neurons, results in resistance to diet-induced obesity. To study the mechanisms by which PPARγ in POMC neurons controls energy balance, we constructed a Cre-recombinase-dependent conditionally activatable transgene expressing either wild-type (WT) or dominant-negative (P467L) PPARγ and the tdTomato reporter. Inducible expression of both forms of PPARγ was validated in cells in culture, in liver of mice infected with an adenovirus expressing Cre-recombinase (AdCre), and in the brain of mice expressing Cre-recombinase either in all neurons (NESCre/PPARγ-P467L) or selectively in POMC neurons (POMCCre/PPARγ-P467L). Whereas POMCCre/PPARγ-P467L mice exhibited a normal pattern of weight gain when fed 60% high-fat diet, they exhibited increased weight gain and fat mass accumulation in response to a 10% fat isocaloric-matched control diet. POMCCre/PPARγ-P467L mice were leptin sensitive on control diet but became leptin resistant when fed 60% high-fat diet. There was no difference in body weight between POMCCre/PPARγ-WT mice and controls in response to 60% high-fat diet. However, POMCCre/PPARγ-WT, but not POMCCre/PPARγ-P467L, mice increased body weight in response to rosiglitazone, a PPARγ agonist. These observations support the concept that alterations in PPARγ-driven mechanisms in POMC neurons can play a role in the regulation of metabolic homeostasis under certain dietary conditions.

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COMPARISON EFFECT OF CV 12, ST 36 AND ST 40 EA ON SHORT TERM ENERGY BALANCE REGULATION IN HIGH FAT DIET RAT

Folia Medica Indonesiana ◽

10.20473/fmi.v52i3.5448 ◽

2017 ◽

Vol 52 (3) ◽

pp. 174

Author(s):

Purwo Sri Rejeki ◽

Harjanto Harjanto ◽

Raden Argarini ◽

Imam Subadi

Keyword(s):

Body Weight ◽

Blood Glucose ◽

Energy Balance ◽

High Fat Diet ◽

Energy Homeostasis ◽

Continuous Wave ◽

Positive Control ◽

Control Group ◽

High Fat ◽

Short Term

The aim of this study was to determine the comparative effects of EA (EA) on the CV12, ST36 and ST40 to weight gain prevention over the short-term regulation of energy balance. The study was conducted with a completely randomized design. Rats were divided into five groups: negative control group (no treatment, n=5), positive control (sham EA/back, n=5), EA CV 12 (n=6), EA ST 36 (n=6) and EA ST 40 (n=7). Rats were exposed to high-fat diet for two weeks and EA was simultaneously performed once daily, five days a week for two weeks with 2 Hz, for 10 minutes with continuous wave. Body weight, BMI, front limb circumference and rear were measured during study. Levels of blood glucose, cholesterol, triglycerides, LDL and HDL were measured at the end of the study; which reflects the short-term regulation of energy homeostasis. For weight loss, EA CV12, ST36 and ST40 group have lost weight significantly compared to the negative and positive control group. The ST40 group has a significant decrease than ST36 and CV12. The most significant decrease in BMI found in the ST40 group. EA did not affect blood glucose levels, but modulated blood lipid profile. In ST 40 group there was a significant decrease in cholesterol, LDL and triglycerides. EA at point ST 40 is potential in preventing increased body weight and BMI in rats exposed to high-fat diet compared to the CV 12 and ST 36. ST 40 is a point with a potential of lowering LDL and triglycerides serum so that it can play a role in the short term regulation of energy homeostasis but also in the prevention of dyslipidemia.

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Neural Protective Effects of Millet and Millet Polyphenols on High-Fat Diet-Induced Oxidative Stress in the Brain

Plant Foods for Human Nutrition ◽

10.1007/s11130-020-00802-6 ◽

2020 ◽

Vol 75 (2) ◽

pp. 208-214 ◽

Cited By ~ 1

Author(s):

Sen Li ◽

Furong Xian ◽

Xiao Guan ◽

Kai Huang ◽

Wenwen Yu ◽

...

Keyword(s):

Oxidative Stress ◽

High Fat Diet ◽

Protective Effects ◽

High Fat ◽

The Brain

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Decrease of Obesity by Allantoin via Imidazoline I1-Receptor Activation in High Fat Diet-Fed Mice

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2013/589309 ◽

2013 ◽

Vol 2013 ◽

pp. 1-7 ◽

Cited By ~ 4

Author(s):

Hsien-Hui Chung ◽

Kung Shing Lee ◽

Juei-Tang Cheng

Keyword(s):

Body Weight ◽

Adipose Tissue ◽

Energy Intake ◽

High Fat Diet ◽

Chronic Administration ◽

Receptor Activation ◽

Inhibitory Effect ◽

High Fat ◽

Epididymal White Adipose Tissue ◽

The Brain

The activation of the imidazoline I1-receptor (I1R) is known to regulate appetite. Allantoin, an active ingredient in the yam, has been reported to improve lipid metabolism in high fat diet- (HFD-)fed mice. However, the effect of allantoin on obesity remains unclear. In the present study, we investigated the effects of allantoin on HFD-induced obesity. The chronic administration of allantoin to HFD-fed mice for 8 weeks significantly decreased their body weight, and this effect was reversed by efaroxan at a dose sufficient to block I1R. The epididymal white adipose tissue (eWAT) cell size and weight in HFD-fed mice were also decreased by allantoin via the activation of I1R. In addition, allantoin significantly decreased the energy intake of HFD-fed mice, and this reduction was associated with a decrease in the NPY levels in the brain. However, no inhibitory effect of allantoin on energy intake was observed in db/db mice. Moreover, allantoin lowered HFD-induced hyperleptinemia, and this activity was abolished by I1R blockade with efaroxan. Taken together, these data suggest that allantoin can ameliorate energy intake and eWAT accumulation by activating I1R to improve HFD-induced obesity.

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Ethyl Acetate Fraction of Amomum xanthioides Ameliorates Nonalcoholic Fatty Liver Disease in a High-Fat Diet Mouse Model

Nutrients ◽

10.3390/nu12082433 ◽

2020 ◽

Vol 12 (8) ◽

pp. 2433

Author(s):

Hwi-Jin Im ◽

Seung-Ju Hwang ◽

Jin-Seok Lee ◽

Sung-Bae Lee ◽

Ji-Yun Kang ◽

...

Keyword(s):

Liver Disease ◽

Mouse Model ◽

Fatty Liver ◽

Ethyl Acetate ◽

Nonalcoholic Fatty Liver Disease ◽

High Fat Diet ◽

Fatty Liver Disease ◽

Ethyl Acetate Fraction ◽

High Fat ◽

Nonalcoholic Fatty Liver

The global prevalence of nonalcoholic fatty liver disease (NAFLD) is estimated to be 25% and has continued to increase; however, no drugs have yet been approved for NAFLD treatments. The ethyl acetate fraction of Amomum xanthioides (EFAX) was previously reported to have an anti-hepatic fibrosis effect, but its effects on steatosis or steatohepatitis remain unclear. This study investigated the anti-fatty liver of EFAX using a high-fat diet mouse model. High-fat diet intake for 8 weeks induced hepatic steatosis with mild inflammation and oxidative damage and increased the adipose tissue weight along with the development of dyslipidemia. EFAX treatment significantly ameliorated the steatohepatic changes, the increased weight of adipose tissues, and the altered serum lipid profiles. These observed effects were possibly due to the lipolysis-dominant activity of EFAX on multiple hepatic proteins including sterol regulatory element-binding protein (mSREBP)-1c, peroxisome proliferator-activated receptor (PPAR)-α, AMP-activated protein kinase, and diglyceride acyltransferases (DGATs). Taken together, these results show that EFAX might be a potential therapeutic agent for regulating a wide spectrum of NAFLDs from steatosis to fibrosis via multiple actions on lipid metabolism-related proteins. Further studies investigating clear mechanisms and their active compounds are needed.

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Hyperpolarized [1-13C] pyruvate MR spectroscopy detect altered glycolysis in the brain of a cognitively impaired mouse model fed high-fat diet

Molecular Brain ◽

10.1186/s13041-018-0415-2 ◽

2018 ◽

Vol 11 (1) ◽

Cited By ~ 3

Author(s):

Young-Suk Choi ◽

Somang Kang ◽

Sang-Yoon Ko ◽

Saeram Lee ◽

Jae Young Kim ◽

...

Keyword(s):

Mouse Model ◽

Mr Spectroscopy ◽

High Fat Diet ◽

Cognitively Impaired ◽

High Fat ◽

The Brain

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Effectiveness of Bioactive Food Components in Experimental Colon Carcinogenesis

Acta Veterinaria Brno ◽

10.2754/avb200978040661 ◽

2009 ◽

Vol 78 (4) ◽

pp. 661-666 ◽

Cited By ~ 3

Author(s):

Emília Hijová ◽

Anna Chmelárová ◽

Alojz Bomba

Keyword(s):

Bile Acid ◽

High Fat Diet ◽

Colon Carcinogenesis ◽

Control Group ◽

Serum Bile Acid ◽

Protective Effects ◽

High Fat ◽

Bile Acid Concentration ◽

Food Components ◽

Bioactive Food Components

The aim of the present study was the evaluation of possible protective effects of selected bioactive food components in experimental N,N-dimethylhydrazine (DMH)-induced colon carcinogenesis. Wistar albino rats (n = 92) were fed a high fat diet or conventional laboratory diet. Two weeks after the beginning of the trial, DMH injections were given to six groups of rats at the dose of 20 mg/kg b.w. twice weekly. The activity of bacterial enzymes in faeces and serum bile acid concentrations were determined. High fat diet, DMH injections, and their combination significantly increased the activies of β-galactosidase, β-glucuronidase, and α-glucosidase (p < 0.001) compared to the control group of rats. Treatment with the prebiotic inulin, Hyppocastani extractum siccum and Lini oleum virginale significantly decreased the activity of β-galactosidase, β-glucuronidase, and α-glucosidase (p < 0.001), as well as the bile acid concentration compared to the group at the highest risk. The protective effects of selected bioactive food components in experimentally induced colon carcinogenesis allow for their possible use in cancer prevention or treatment.

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