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Background: Maltose is a disaccharide formed from two units of glucose. The amount of maltose in raw sweet potatoes reportedly increased by more than 40-fold after baking. We aimed to investigate the effects of maltose consumption on diet-induced obesity using a mouse model. Methods: Male C57BL/6J mice were divided into three dietary groups: a control diet of American Institute of Nutrition (AIN)-93 (CD), an AIN-93-based 30% high-fat diet (HFD), or an HFD diet containing 7.0% maltose (HFD+Mal). After 13 weeks, body mass index, blood glucose, lipid parameters, including total cholesterol and triglyceride, and hepatic fatty acid content were evaluated. Results: After 6 weeks on the special diet, weight gain was significantly higher in the HFD+Mal group than in the HFD group. The body mass index rose steadily and was significantly higher in the HFD+Mal group (5.03 ± 0.22), compared to the CD (3.32 ± 0.30) and HFD (4.57 ± 0.40) groups at 12 weeks. The relative liver weight per weight was also significantly higher in the HFD+Mal group than in the other two groups. The increases in blood glucose levels were more significant in the HFD+Mal group compared to the HFD group, as were the plasma levels of total cholesterol, high-density lipoprotein (HDL)-cholesterol and non-HDL-cholesterol. In the liver, levels of the following fatty acids increased in both the HFD and HFD+Mal groups relative to those in the CD group: C14:0 (myristic acid), C16:0 (palmitic acid), C18:0 (stearic acid), C18:1 (oleic acid), C18:2 (linoleic acid) and C18:3 (α-linolenic acid). Additionally, the C16:0 content in the HFD+Mal group was significantly higher than that in the HFD group. Conclusion: The results of this study suggest that daily consumption of maltose exacerbated the development of obesity and related parameters, including body mass index and plasma cholesterol levels, under the high-fat diet consumption. It is possible that the consumption of maltose-rich cooked sweet potatoes, as part of an overall HFD, might exacerbate HFD-induced overweight. [ABSTRACT FROM AUTHOR]

In our study, we investigated whether Aster yomena (Kitam.) Honda (AY) improved cognitive impairment which results from consumption of high‐fat diet (HFD). When ethyl acetate fraction from AY (EFAY) was administered to C57BL/6J mice fed with 60% HFD, EFAY significantly enhanced cognitive ability that was impaired by HFD in T‐maze test and novel object recognition test. Furthermore, EFAY increased memory and learning functions that were proven during Morris water maze test. We further elucidated protective mechanisms of EFAY against cognitive decline that resulted from obesity by western blotting. In the brain, HFD increased neuronal inflammation and disturbed insulin receptor substrate‐1 (IRS‐1)/Akt pathway. However, EFAY significantly downregulated inflammation‐related protein expressions such as nuclear factor‐κB interleukin‐1β, inducible nitric oxide synthase and cyclooxygenase‐2, compared with the HFD‐fed control group. Furthermore, the IRS‐1/Akt pathway was regulated by EFAY, indicating that EFAY ameliorated insulin resistance in the brain. Practical applications: Obesity and its complications increase the risk for developing cognitive dysfunction such as dementia. Administration of ethyl acetate fraction from AY (EFAY)‐attenuated cognitive and memory impairment by inhibitions of neuronal oxidative stress and low‐grade chronic inflammation in high‐fat diet (HFD)‐induced cognitive impairment mouse model. In addition, EFAY‐administered mice disturbed cerebral insulin receptor substrate‐1 (IRS‐1)/Akt pathway. These data suggest that EFAY‐improved cognitive impairment induced by HFD through modulation of insulin resistance and inflammation. Therefore, we proposed that AY could be a potential agent to prevent cognitive dysfunction induced by obesity and insulin resistance. [ABSTRACT FROM AUTHOR]

Objective: To explore the effects of the quinoa diet on glycolipid metabolism and endoplasmic reticulum (ER) stress in an obese mouse model. Methods: Six-week-old C57BL/6J female mice have received a high-fat diet (HFD) to induce obesity and subsequently were treated with a quinoa diet for 12 weeks. During this period, fasting blood glucose, body fat and insulin resistance were measured regularly. At the end of the experiment, mouse serum and liver tissue were collected. The differences in glucose and lipid metabolism were analyzed, and liver tissue pathological morphology, liver endoplasmic reticulum stress-related mRNA and protein levels, and serum oxidative stress levels were measured. Results: Quinoa diet could significantly reduce the level of blood glucose, triglyceride, cholesterol, low-density lipoprotein, improve glucose tolerance, as well as improve histological changes of liver tissues in obese mice (P < 0.05 or < 0.01). Besides, quinoa could improve oxidative stress indicators such as GSH, and MDA (P < 0.05 or < 0.01). Furthermore, quinoa can down-regulate mRNA expression of ER stress markers eIF2α, GRP78, and CHOP in the liver of obese mice (P < 0.05 or < 0.01). Conclusions: Quinoa supplementation can improve glycolipid metabolism, regulate ER stress, and alleviate obesity in HFD-induced mice. [ABSTRACT FROM AUTHOR]

Quercetin has been shown to have anti-obesity effects, but it is unknown whether these effects can be transmitted from mothers to their progeny. In this study, we investigated whether maternal quercetin consumption during pregnancy has a protective effect on high-fat diet–induced hyper lipid levels and overweight in progeny. Female mice consumed a control diet or a diet containing 1.0% quercetin during breeding. The male progeny were then divided into four groups that were (1) sacrificed at postnatal day 3; (2) born to dams fed the control diet and also fed the control diet (C-C), (3) born to dams fed the control diet and then fed a 30% high-fat diet (C-HF), or (4) born to dams fed the Q-diet and then fed the HF diet (Q-HF). Maternal consumption of quercetin did not affect body weight or blood lipid parameters in either dams or neonates at postnatal day 3. After 13 weeks, the Q-HF group exhibited greater body and liver weights, and higher blood cholesterol levels than the C-HF group. However, the total cholesterol/ high density lipoprotein (HDL)-cholesterol ratios in the Q-HF and C-C groups remained similar. In conclusion, maternal quercetin consumption does not appear to protect the next generation from high-fat diet–induced hyper cholesterol level in the blood and liver, and consequently overweight, but may help regulate the total cholesterol/HDL-cholesterol ratio.

Black-fruited chokeberries (Aronia melanocarpa), growing mainly in the Central and Eastern European countries, have health benefits due to the high concentrations of polyphenolic compounds. However, a strong bitter taste of chokeberries limits its usage as functional food. We hypothesized that the fermented A. melanocarpa with a reduced bitter taste would improve insulin sensitivity and/or ameliorate weight gain induced by high-fat diet (HFD) in male C57BL/6J mice. The mice were administered with HFD together with the 100 mg/kg of natural A. melanocarpa (T1) or the fermented A. melanocarpa (T2) for 8 weeks. The treatment with T2 (100 mg/kg body weight, p.o.) markedly attenuated the weight gain and the increase in serum triglyceride level induced by HFD. The T2-treated group had better glucose tolerance and higher insulin sensitivity as measured by oral glucose tolerance test and intraperitoneal insulin tolerance test in comparison to the T1-treated group. Phytochemical analysis revealed that the main constituents of T2 were cyanidin-3-xyloside and 1-(3′,4′-dihydroxycinnamoyl)cyclopenta-2,3-diol, and the content of cyanidin glycosides (3-glucoside, 3-xyloside) was significantly reduced during the fermentation process. From the above results, we postulated that antiobesity effect of black chokeberry was not closely correlated with the cyanidin content. Fermented chokeberry might be a viable dietary supplement rich in bioactive compounds useful in preventing obesity. [ABSTRACT FROM AUTHOR]

Although the serine active site containing 1 (SERAC1) protein is essential for cardiolipin remodeling and cholesterol transfer, its physiological role in whole-body energy metabolism remains unclear. Thus, we investigated the role of SERAC1 in lipid distribution and metabolism in mice. CRISPR/Cas9 was used to create homozygous Serac1 knockout mice. A range of methods, including electron microscopy, histological analysis, DNA sequencing, glucose and insulin tolerance tests, and biochemical analysis of serum lipid levels, were used to assess lipid distribution and rates of lipid synthesis in mice. We found that Serac1 depletion in mice prevented high-fat diet-induced obesity but did not affect energy expenditure. The liver was affected by Serac1 depletion, but adipose tissues were not. Serac1 depletion was shown to impair cholesterol transfer from the liver to the serum and led to an imbalance in cholesterol distribution. The livers from mice with Serac1 depletion showed increased cholesterol synthesis because the levels of cholesterol synthesis enzymes were upregulated. Moreover, the accumulation of hepatic lipid droplets in mice with Serac1 depletion were decreased, suggesting that SERAC1 depletion may decrease the risk for hepatic steatosis in high fat diet-induced mice. Our findings demonstrate that SERAC1 can serve as a potential target for the treatment or prevention of diet-induced hepatic lipid metabolic disorders. [Display omitted] • SERAC1 alters lipid metabolism in the liver of mice. • SERAC1 deletion protects against high fat diet-induced obesity in mice. • SERAC1 deletion alters the synthesis and storage of cholesterol in the liver of HFD-fed mice. [ABSTRACT FROM AUTHOR]

d -Xylose, a natural pentose, has been reported to reduce postprandial glucose levels, although its effect on lipid metabolism has not been investigated. Therefore, this study hypothesized that d -xylose, as an alternative sweetener, suppresses adipogenesis and lipid metabolism by regulating blood lipid profiles, blood glucose levels, and related gene expression in high-fat diet (HFD)–induced obese mice. Mice were fed a normal diet, a 60% HFD diet, or an HFD with 5% or 10% of the total sucrose content supplemented with d -xylose (Xylo 5 and Xylo 10 diets, respectively). Weight gain, food intake, and serum lipid levels for each group were measured. After 12 weeks, histopathology of liver sections and assays of gene expression related to adipogenesis and lipid metabolism in visceral fat and liver tissues were analyzed. Body weight gain; fasting blood glucose levels; weights of subcutaneous and visceral adipose tissues; and serum biochemical markers, including total cholesterol and low-density lipoprotein cholesterol, low-/high-density lipoprotein, and total cholesterol/high-density lipoprotein, were significantly lowered in the Xylo 5 and Xylo 10 groups. In addition, d -xylose supplementation resulted in the down-regulation of adipogenesis-related genes, including sterol regulatory element-binding protein 1C, fatty acid synthase, adipocyte protein 2, and CCAAT/enhancer-binding protein α in visceral adipose tissues. Histopathologically, Xylo 5 and Xylo 10 supplementation reduced HFD-induced fat accumulation in the liver and decreased expressions of fatty acid synthase and peroxisome proliferator-activated receptor γ . d -Xylose supplementation also enhanced lipid oxidation by increasing expressions of carnitine palmitoyltransferase 1A; cytochrome P450, family 4, subfamily a, polypeptide 10; and acyl-CoA oxidase. In conclusion, our finding suggests that d -xylose may help prevent or attenuate the progression of obesity-related metabolic disorders by alleviating adipogenesis and dyslipidemia and improving lipid oxidation. [ABSTRACT FROM AUTHOR]

The purpose of this study was to examine the antiobesity effects of Monascus pilosus-fermented black soybean (F-BS) in C57BL/6 mice with high-fat diet (HFD)-induced obesity. F-BS (oral, 0.5 and 1.0 g/kg per body weight, twice per day) ameliorated obesity by reducing body and liver weight increases, and regulating blood glucose and cholesterol levels in C57BL/6 mice fed a control or HFD with oral administration of F-BS for 12 weeks. F-BS suppressed the growth of epididymal, retroperitoneal, and perirenal fat pads by preventing increases in the adipocyte size. Moreover, the levels of blood glucose, total cholesterol, and leptin were significantly lowered by F-BS administration in a dose-dependent manner. These results indicated that F-BS is a beneficial food supplement for preventing obesity, controlling blood glucose, and lowering cholesterol. Future research strategies should address the mechanisms that selectively regulate obesity, including hyperglycemia and hypercholesterolemia. [ABSTRACT FROM AUTHOR]

Abstract: Consumption of a high-fat diet (HFD) is correlated with increased oxidative stress and chronic inflammation in many organs. Regulatory T cells (Tregs) are essential negative regulators of inflammation. We hypothesized that resveratrol (trans-3,5,4′-trihydroxystilbene) could protect against HFD-induced oxidative stress and inflammation. Therefore, we examined the effect of resveratrol on oxidative stress and the relevant peripheral immune-regulating mechanisms in HFD-induced obese (DIO) and diet-resistant mice. C57BL/6 mice were fed a normal diet and an HFD for 13 weeks. Then the experimental group was subdivided into DIO and diet-resistant groups according to their body weights, which were further supplemented with 0.03% resveratrol and 0.06% resveratrol, respectively, for an additional 13 weeks. Resveratrol prevented the accumulation of chronic oxidative stress and suppression of Tregs production in HFD mice, modulated changes of cytokines in the plasma and spleen, and decreased expressions of inflammatory mediators compared with those of the DIO group. Our results indicate that resveratrol, as a feasible effective supplement for HFD, can relieve oxidative stress, inhibit inflammatory genes expression, and increase Tregs number via aryl hydrocarbon receptor activation inhibited by HFD, especially in DIO mice. [Copyright &y& Elsevier]

Quercetin has been shown to have anti-obesity effects, but it is unknown whether these effects can be transmitted from mothers to their progeny. In this study, we investigated whether maternal quercetin consumption during pregnancy has a protective effect on high-fat diet–induced hyper lipid levels and overweight in progeny. Female mice consumed a control diet or a diet containing 1.0% quercetin during breeding. The male progeny were then divided into four groups that were (1) sacrificed at postnatal day 3; (2) born to dams fed the control diet and also fed the control diet (C-C), (3) born to dams fed the control diet and then fed a 30% high-fat diet (C-HF), or (4) born to dams fed the Q-diet and then fed the HF diet (Q-HF). Maternal consumption of quercetin did not affect body weight or blood lipid parameters in either dams or neonates at postnatal day 3. After 13 weeks, the Q-HF group exhibited greater body and liver weights, and higher blood cholesterol levels than the C-HF group. However, the total cholesterol/ high density lipoprotein (HDL)-cholesterol ratios in the Q-HF and C-C groups remained similar. In conclusion, maternal quercetin consumption does not appear to protect the next generation from high-fat diet–induced hyper cholesterol level in the blood and liver, and consequently overweight, but may help regulate the total cholesterol/HDL-cholesterol ratio. [ABSTRACT FROM AUTHOR]