Mori Folium and Mori Fructus Mixture Attenuates High-Fat Diet-Induced Cognitive Deficits in Mice

Obesity has become a global health problem, contributing to various diseases including diabetes, hypertension, cancer, and dementia. Increasing evidence suggests that obesity can also cause neuronal damage, long-term memory loss, and cognitive impairment. The leaves and the fruits ofMorus albaL., containing active phytochemicals, have been shown to possess antiobesity and hypolipidemic properties. Thus, in the present study, we assessed their effects on cognitive functioning in mice fed a high-fat diet by performing immunohistochemistry, using antibodies against c-Fos, synaptophysin, and postsynaptic density protein 95 and a behavioral test. C57BL/6 mice fed a high-fat diet for 21 weeks exhibited increased body weight, but mice coadministered an optimized Mori Folium and Mori Fructus extract mixture (2 : 1; MFE) for the final 12 weeks exhibited significant body weight loss. Additionally, obese mice exhibited not only reduced neural activity, but also decreased presynaptic and postsynaptic activities, while MFE-treated mice exhibited recovery of these activities. Finally, cognitive deficits induced by the high-fat diet were recovered by cotreatment with MFE in the novel object recognition test. Our findings suggest that the antiobesity effects of MFE resulted in recovery of the cognitive deficits induced by the high-fat diet by regulation of neural and synaptic activities.

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Ameliorative Effect of Hexane Extract ofPhalaris canariensison High Fat Diet-Induced Obese and Streptozotocin-Induced Diabetic Mice

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2014/145901 ◽

2014 ◽

Vol 2014 ◽

pp. 1-13 ◽

Cited By ~ 8

Author(s):

Rosa Martha Perez Gutierrez ◽

Diana Madrigales Ahuatzi ◽

Maria del Carmen Horcacitas ◽

Efren Garcia Baez ◽

Teresa Cruz Victoria ◽

...

Keyword(s):

Oxidative Stress ◽

Body Weight ◽

High Fat Diet ◽

Serum Insulin ◽

Body Weight Loss ◽

Insulin Level ◽

Hexane Extract ◽

Diabetic Mice ◽

High Fat ◽

Obesity And Diabetes

Obesity is one of the major factors to increase various disorders like diabetes. The present paper emphasizes study related to the antiobesity effect ofPhalaris canariensisseeds hexane extract (Al-H) in high-fat diet- (HFD-) induced obese CD1 mice and in streptozotocin-induced mild diabetic (MD) and severely diabetic (SD) mice.AL-H was orally administered to MD and SD mice at a dose of 400 mg/kg once a day for 30 days, and a set of biochemical parameters were studied: glucose, cholesterol, triglycerides, lipid peroxidation, liver and muscle glycogen, ALP, SGOT, SGPT, glucose-6-phosphatase, glucokinase, hexokinase, SOD, CAT, GSH, GPX activities, and the effect on insulin level. HS-H significantly reduced the intake of food and water and body weight loss as well as levels of blood glucose, serum cholesterol, triglyceride, lipoprotein, oxidative stress, showed a protective hepatic effect, and increased HDL-cholesterol, serum insulin in diabetic mice. The mice fed on the high-fat diet and treated with AL-H showed inhibitory activity on the lipid metabolism decreasing body weight and weight of the liver and visceral adipose tissues and cholesterol and triglycerides in the liver. We conclude that AL-H can efficiently reduce serum glucose and inhibit insulin resistance, lipid abnormalities, and oxidative stress in MD and SD mice. Our results demonstrate an antiobesity effect reducing lipid droplet accumulation in the liver, indicating that its therapeutic properties may be due to the interaction plant components soluble in the hexane extract, with any of the multiple targets involved in obesity and diabetes pathogenesis.

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The PYY/Y2R-Deficient Mouse Responds Normally to High-Fat Diet and Gastric Bypass Surgery

10.20944/preprints201902.0100.v1 ◽

2019 ◽

Author(s):

Brandon Boland ◽

Michael B. Mumphrey ◽

Zheng Hao ◽

Benji Gill ◽

R. Leigh Townsend ◽

...

Keyword(s):

Gastric Bypass ◽

Body Composition ◽

Body Weight ◽

High Fat Diet ◽

Body Weight Loss ◽

Liver Weight ◽

Receptor Subtypes ◽

High Fat ◽

Knockout Mouse Model ◽

Gut Hormone

Background/Goals: The gut hormone PYY secreted from intestinal L-cells has been implicated in the mechanisms of satiation via Y2-receptor (Y2R) signaling in the brain and periphery and is a major candidate for mediating the beneficial effects of bariatric surgery on appetite and body weight. Methods: Here we assessed the role of Y2R signaling in the response to low- and high-fat diets and its role in the effects of Roux-en-Y gastric bypass (RYGB) surgery on body weight, body composition, food intake, energy expenditure and glucose handling, in global Y2R-deficient (Y2RKO) and wildtype mice made obese on high-fat diet. Results: Both male and female Y2RKO mice responded normally to low- and high-fat diet in terms of body weight, body composition, fasting levels of glucose and insulin, as well as glucose and insulin tolerance for up to 30 weeks of age. Contrary to expectations, obese Y2RKO mice also responded similarly to RYGB compared to WT mice for up to 20 weeks after surgery, with initial hypophagia, sustained body weight loss, and significant improvements in fasting insulin, glucose tolerance, HOMA-IR, and liver weight compared to sham-operated mice. Furthermore, non-surgical Y2RKO mice weight-matched to RYGB showed the same improvements in glycemic control as Y2RKO mice with RYGB that were similar to WT mice. Conclusions: PYY signaling through Y2R is not required for the normal appetite-suppressing and body weight-lowering effects of RYGB in this global knockout mouse model. Potential compensatory adaptations of PYY signaling through other receptor subtypes or other gut satiety hormones such as GLP-1 remain to be investigated.

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The PYY/Y2R-Deficient Mouse Responds Normally to High-Fat Diet and Gastric Bypass Surgery

Nutrients ◽

10.3390/nu11030585 ◽

2019 ◽

Vol 11 (3) ◽

pp. 585 ◽

Cited By ~ 6

Author(s):

Brandon Boland ◽

Michael Mumphrey ◽

Zheng Hao ◽

Benji Gill ◽

R. Townsend ◽

...

Keyword(s):

Gastric Bypass ◽

Body Composition ◽

Body Weight ◽

High Fat Diet ◽

Peptide Yy ◽

Body Weight Loss ◽

Receptor Subtypes ◽

High Fat ◽

Knockout Mouse Model ◽

Gut Hormone

Background/Goals: The gut hormone peptide YY (PYY) secreted from intestinal L-cells has been implicated in the mechanisms of satiation via Y2-receptor (Y2R) signaling in the brain and periphery and is a major candidate for mediating the beneficial effects of bariatric surgery on appetite and body weight. Methods: Here we assessed the role of Y2R signaling in the response to low- and high-fat diets and its role in the effects of Roux-en-Y gastric bypass (RYGB) surgery on body weight, body composition, food intake, energy expenditure and glucose handling, in global Y2R-deficient (Y2RKO) and wildtype (WT) mice made obese on high-fat diet. Results: Both male and female Y2RKO mice responded normally to low- and high-fat diet in terms of body weight, body composition, fasting levels of glucose and insulin, as well as glucose and insulin tolerance for up to 30 weeks of age. Contrary to expectations, obese Y2RKO mice also responded similarly to RYGB compared to WT mice for up to 20 weeks after surgery, with initial hypophagia, sustained body weight loss, and significant improvements in fasting insulin, glucose tolerance, insulin resistance (HOMA-IR), and liver weight compared to sham-operated mice. Furthermore, non-surgical Y2RKO mice weight-matched to RYGB showed the same improvements in glycemic control as Y2RKO mice with RYGB that were similar to WT mice. Conclusions: PYY signaling through Y2R is not required for the normal appetite-suppressing and body weight-lowering effects of RYGB in this global knockout mouse model. Potential compensatory adaptations of PYY signaling through other receptor subtypes or other gut satiety hormones such as glucagon-like peptide-1 (GLP-1) remain to be investigated.

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High-fat diet induces site-specific unresponsiveness to LPS-stimulated STAT3 activation in the hypothalamus

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00147.2013 ◽

2014 ◽

Vol 306 (1) ◽

pp. R34-R44 ◽

Cited By ~ 7

Author(s):

Beatriz de Carvalho Borges ◽

Rodrigo Rorato ◽

Ernane Torres Uchoa ◽

Paula Marangon ◽

Glauber S. F. da Silva ◽

...

Keyword(s):

Weight Loss ◽

Body Weight ◽

Food Intake ◽

Energy Expenditure ◽

Brain Stem ◽

High Fat Diet ◽

Control Diet ◽

Body Weight Loss ◽

Hypothalamic Nucleus ◽

High Fat

Hypophagia induced by inflammation is associated with Janus kinase (JAK)-2/signal transducer and activator of transcription (STAT) 3 signaling pathway, and leptin-mediated hypophagia is also mediated by JAK2-STAT3 pathway. We have previously reported that lipopolysaccharide (LPS) did not reduce food intake in leptin-resistant high-fat diet (HFD) rats but maintained body weight loss. We investigated whether changes in p-STAT3 expression in the hypothalamus and brain stem could account for the desensitization of hypophagia in HFD animals after a low LPS dose (100 μg/kg). Wistar rats fed standard diet (3.95 kcal/g) or HFD (6.3 kcal/g) for 8 wk were assigned into control diet-saline, control diet-LPS, HFD-saline, and HFD-LPS groups. LPS reduced feeding in the control diet but not HFD. This group showed no p-STAT3 expression in the paraventricular nucleus (PVN) and ventromedial hypothalamic nucleus (VMH), but sustained, though lower than control, p-STAT3 in the nucleus of the solitary tract (NTS) and raphe pallidus (RPa). LPS decreased body weight in HFD rats and increased Fos expression in the NTS. LPS increased body temperature, oxygen consumption, and energy expenditure in both control diet and HFD rats, and this response was more pronounced in HFD-LPS group. Brown adipose tissue (BAT) thermogenesis and increased energy expenditure seem to contribute to body weight loss in HFD-LPS. This response might be related with increased brain stem activation. In conclusion, LPS activates STAT3-mediated pathway in the hypothalamus and brain stem, leading to hypophagia, however, LPS effects on food intake, but not body weight loss, are abolished by leptin resistance induced by HFD. The preserved STAT3 phosphorylation in the brain stem suggests that unresponsiveness to LPS on STAT3 activation under HFD might be selective to the hypothalamus.

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Thymoquinone Protects Neurons in the Cerebellum of Rats through Mitigating Oxidative Stress and Inflammation Following High-Fat Diet Supplementation

Biomolecules ◽

10.3390/biom11020165 ◽

2021 ◽

Vol 11 (2) ◽

pp. 165

Author(s):

Aziza Alrafiah

Keyword(s):

Oxidative Stress ◽

Body Weight ◽

High Fat Diet ◽

Neuronal Damage ◽

Morphological Changes ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

The Body ◽

Control Group ◽

High Fat

High-fat diet (HFD) is a major problem causing neuronal damage. Thymoquinone (TQ) could regulate oxidative stress and the inflammatory process. Hence, the present study elucidated the significant role of TQ on oxidative stress, inflammation, as well as morphological changes in the cerebellum of rats with HFD. Rats were divided into three groups as (1) control, (2) saturated HFD for eight weeks and (3) HFD supplementation (four weeks) followed by TQ 300 mg/kg/day treated (four weeks). After treatment, blood samples were collected to measure oxidative stress markers glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), and inflammatory cytokines. Furthermore, neuronal morphological changes were also observed in the cerebellum of the rats. HFD rats show higher body weight (286.5 ± 7.4 g) as compared with the control group (224.67 ± 1.78 g). TQ treatment significantly (p < 0.05) lowered the body weight (225.83 ± 13.15 g). TQ produced a significant (p < 0.05) reduction in cholesterol, triglycerides, high-density lipoprotein (HDL), and low-density lipoprotein (LDL). The antioxidative enzymes significantly reduced in HFD rats (GSH, 1.46 ± 0.36 mol/L and SOD, 99.13 ± 5.41 µmol/mL) as compared with the control group (GSH, 6.25 ± 0.36 mol/L and SOD, 159.67 ± 10.67 µmol/mL). MDA was increased significantly in HFD rats (2.05 ± 0.25 nmol/L) compared to the control group (0.695 ± 0.11 nmol/L). Surprisingly, treatment with TQ could improve the level of GSH, MDA, and SOD. TQ treatment significantly (p < 0.05) reduced the inflammatory markers as compared with HFD alone. TQ treatment minimizes neuronal damage as well as reduces inflammation and improves antioxidant enzymes. TQ can be considered as a promising agent in preventing the neuronal morphological changes in the cerebellum of obese populations.

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Central NMU signaling in body weight and energy balance regulation: evidence from NMUR2 deletion and chronic central NMU treatment in mice

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.91022.2008 ◽

2009 ◽

Vol 297 (3) ◽

pp. E708-E716 ◽

Cited By ~ 14

Author(s):

Emil Egecioglu ◽

Karolina Ploj ◽

Xiufeng Xu ◽

Mikael Bjursell ◽

Nicolas Salomé ◽

...

Keyword(s):

Body Weight ◽

Energy Balance ◽

High Fat Diet ◽

Body Weight Loss ◽

Standard Diet ◽

Wild Type ◽

High Fat ◽

Gene Encoding ◽

Male And Female

To investigate the role of the central neuromedin U (NMU) signaling system in body weight and energy balance regulation, we examined the effects of long-term intracerebroventricular (icv) infusion of NMU in C57Bl/6 mice and in mice lacking the gene encoding NMU receptor 2. In diet-induced obese male and female C57BL/6 mice, icv infusion of NMU (8 μg·day−1·mouse−1) for 7 days decreased body weight and total energy intake compared with vehicle treatment. However, these parameters were unaffected by NMU treatment in lean male and female C57BL/6 mice fed a standard diet. In addition, female (but not male) NMUR2-null mice had increased body weight and body fat mass when fed a high-fat diet but lacked a clear body weight phenotype when fed a standard diet compared with wild-type littermates. Furthermore, female (but not male) NMUR2-null mice fed a high-fat diet were protected from central NMU-induced body weight loss compared with littermate wild-type mice. Thus, we provide the first evidence that long-term central NMU treatment reduces body weight, food intake, and adiposity and that central NMUR2 signaling is required for these effects in female but not male mice.

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Adiponectin promoter activator NP-1 reduces body weight and hepatic steatosis in high-fat diet-fed animals

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00468.2011 ◽

2012 ◽

Vol 302 (7) ◽

pp. E817-E830 ◽

Cited By ~ 8

Author(s):

Antonia Serrano ◽

Francisco J. Pavón ◽

Juan Suarez ◽

Patricia Rivera ◽

Margarita Vida ◽

...

Keyword(s):

Body Weight ◽

High Fat Diet ◽

Body Weight Gain ◽

Liver Steatosis ◽

Body Weight Loss ◽

Acute Administration ◽

High Fat ◽

Nonalcoholic Fatty Liver ◽

Diet Induced Obesity

Enhancement of adiponectin level has been shown to have beneficial effects, including antiobesity, antidiabetic, and hepatoprotective effects. This evidence supports the therapeutic utility of adiponectin in complicated obesity. The present study characterized the in vivo effects of sustained adiponectin release by NP-1, a new class of thiazol derivative that increases adiponectin levels. Acute administration of NP-1 reduced feeding, increased plasma adiponectin, and improved insulin sensitivity without inducing malaise, as revealed by conditioned taste aversion studies. Short-term (7 days) treatment with NP-1 also reduced feeding and body weight gain and increased phosphorylation of AMPK in muscle, a main intracellular effector of adiponectin. NP-1 was also evaluated in diet-induced obesity, and adult male Wistar rats were fed two different types of diet: a standard high-carbohydrate/low-fat diet (SD) and a high-fat diet (HFD). Once obesity was established, animals were treated daily with NP-1 (5 mg/kg) for 14 consecutive days. Chronic NP-1 induced body weight loss and reduction of food intake and resulted in both a marked decrease in liver steatosis and an improvement of biochemical indexes of liver damage in HFD-fed rats. However, a marked induction of tolerance in adiponectin gene transcription and release was observed after chronic NP-1 with respect to the acute actions of this drug. The present results support the role of adiponectin signaling in diet-induced obesity and set in place a potential use of compounds able to induce adiponectin release for the treatment of obesity and nonalcoholic fatty liver, with the limits imposed by the induction of pharmacological tolerance.

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The effects of enterostatin intake on food intake and energy expenditure

British Journal Of Nutrition ◽

10.1079/bjn2003871 ◽

2003 ◽

Vol 90 (1) ◽

pp. 207-214 ◽

Cited By ~ 15

Author(s):

Eva M. R. Kovacs ◽

Manuela P. G. M. Lejeune ◽

Margriet S. Westerterp-Plantenga

Keyword(s):

Body Weight ◽

Food Intake ◽

Energy Expenditure ◽

High Fat Diet ◽

Resting Metabolic Rate ◽

Body Weight Loss ◽

Negative Energy ◽

High Fat ◽

Double Blind ◽

Diet Induced Thermogenesis

Enterostatin (ENT) has been found to inhibit food intake and selectively inhibit fat intake in rats. Both peripheral and central mechanisms have been proposed. It also has been suggested that ENT may increase thermogenesis. The present study investigated the effects of oral ENT administration on food intake, energy expenditure and body weight in subjects with a preference for a high-fat diet. In a double-blind, placebo-controlled, randomized and crossover design, nine female and three male healthy subjects (age 34 (sd 11) years, BMI 24·5 (sd 2·5) kg/m2) with a preference for a high-fat diet ingested ENT (3 × 15 mg/d) or placebo (PLA) while consuming a high-fat diet ad libitum for 4d. Eight subjects ended each intervention with a 36h stay in the respiration chamber, continuing the diet and treatment. Body-weight loss was significant (ENT 0·8 (se 0·3) kg, P<0·05; PLA 1·3 (se 0·3) kg, P<0·001), but not different between treatments. There was no difference between treatments in total energy intake (ENT 37·1 (se 2·6), PLA 35·9 (se 3·2) MJ), macronutrient composition, hunger, satiety and hedonic scores during the 4d high-fat diet. Energy expenditure (24h) (ENT 9·6 (se 0·4), PLA 9·5 (se 0·4) MJ), sleeping and resting metabolic rate, diet-induced thermogenesis, activity-induced energy expenditure and 24h RQ (ENT 0·77 (se 0·01), PLA 0·77 (se 0·01)) were similar for both treatments. We conclude that oral ENT administration did not affect food intake, energy expenditure or body weight in subjects with a preference for a high-fat diet experiencing a negative energy and fat balance.

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