Nutrients

Editorial

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4 pages, 217 KiB

Open AccessEditorial

New Insights into High-Fat Diet with Chronic Diseases

by Xiaoyu Wang, Rui Song, Maëlys Clinchamps and Frédéric Dutheil

Nutrients 2023, 15(18), 4031; https://doi.org/10.3390/nu15184031 - 18 Sep 2023

Cited by 2 | Viewed by 1916

Abstract

Chronic diseases, encompassing conditions such as heart disease, cancer, and diabetes, represent a significant global health challenge and are the leading causes of mortality worldwide [...] Full article

(This article belongs to the Special Issue High Fat Diet with Chronic Diseases)

Research

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19 pages, 6811 KiB

Open AccessArticle

Standardized Ethanol Extract of Cassia mimosoides var. nomame Makino Ameliorates Obesity via Regulation of Adipogenesis and Lipogenesis in 3T3-L1 Cells and High-Fat Diet-Induced Obese Mice

by So-Won Heo, Kyung-Sook Chung, Young-Seo Yoon, Soo-Yeon Kim, Hye-Shin Ahn, Yu-Kyong Shin, Sun-Hee Lee and Kyung-Tae Lee

Nutrients 2023, 15(3), 613; https://doi.org/10.3390/nu15030613 - 25 Jan 2023

Cited by 11 | Viewed by 3416

Abstract

Obesity is a major cause of conditions such as type 2 diabetes and non-alcoholic fatty liver disease, posing a threat to public health worldwide. Here, we analyzed the anti-obesity effects of a standardized ethanol extract of Cassia mimosoides var. nomame Makino (EECM) in [...] Read more.

Obesity is a major cause of conditions such as type 2 diabetes and non-alcoholic fatty liver disease, posing a threat to public health worldwide. Here, we analyzed the anti-obesity effects of a standardized ethanol extract of Cassia mimosoides var. nomame Makino (EECM) in vitro and in vivo. Treatment of 3T3-L1 adipocytes with EECM suppressed adipogenesis and lipogenesis via the AMP-activated protein kinase pathway by downregulating the expression levels of CCAAT/enhancer-binding protein-alpha, peroxisome proliferator-activated receptor (PPAR)-γ, sterol regulatory element-binding protein-1, and fatty acid synthase and upregulating the acetyl-CoA carboxylase. EECM inhibited mitotic clonal expansion during early adipocyte differentiation. Oral administration of EECM for 10 weeks significantly alleviated body weight gain and body fat accumulation in high-fat diet (HFD)-fed mice. EECM mitigated adipogenesis and lipid accumulation in white adipose and liver tissues of HFD-induced obese mice. It regulated the levels of adipogenic hormones including insulin, leptin, and adipokine in the blood plasma. In brown adipose tissue, EECM induced the expression of thermogenic factors such as uncoupling protein-1, PPAR-α, PPARγ co-activator-1α, sirtuin 1, and cytochrome c oxidase IV. EECM restored the gut microbiome composition at the phylum level and alleviated dysbiosis. Therefore, EECM may be used as a promising therapeutic agent for the prevention of obesity. Full article

(This article belongs to the Special Issue High Fat Diet with Chronic Diseases)

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10 pages, 1449 KiB

Open AccessArticle

High-Calorie Food-Cues Impair Conflict Control: EEG Evidence from a Food-Related Stroop Task

by Yong Liu, Jia Zhao, Yizhou Zhou, Ruiyu Yang, Beichen Han, Yufei Zhao, Yazhi Pang, Hong Yuan and Hong Chen

Nutrients 2022, 14(21), 4593; https://doi.org/10.3390/nu14214593 - 1 Nov 2022

Cited by 5 | Viewed by 2313

Abstract

Long-term excessive intake of high-calorie foods might lead to cognitive impairments and overweight or obesity. The current study aimed to examine the effects of high-calorie foods on the behavioral and neurological correlates of food-related conflict control ability. A food-related Stroop task, which asked [...] Read more.

Long-term excessive intake of high-calorie foods might lead to cognitive impairments and overweight or obesity. The current study aimed to examine the effects of high-calorie foods on the behavioral and neurological correlates of food-related conflict control ability. A food-related Stroop task, which asked the participants to respond to the food images and ignore the calorie information, were employed. A total of 61 individuals were recruited and who completed the food-related Stroop task with event-related potentials (ERPs). Participants exhibited a slower reaction time and lower accuracy in high-calorie food stimuli than that in low-calorie food stimuli. The ERP results exhibited a reduction in N2 amplitudes when responding to high-calorie food stimuli compared to when responding to low-calorie food stimuli. In addition, time-frequency analysis revealed that theta power induced by low-calorie food stimuli was significantly greater than that of high-calorie food stimuli. The findings indicated that high-calorie foods impair food-related conflict control. The present study expands on the previous studies of the neural correlates of food cues and provides new insights into the processing and resolving of conflicting information for eating behavior and weight control. Full article

(This article belongs to the Special Issue High Fat Diet with Chronic Diseases)

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14 pages, 3821 KiB

Open AccessArticle

Nova1 or Bim Deficiency in Pancreatic β-Cells Does Not Alter Multiple Low-Dose Streptozotocin-Induced Diabetes and Diet-Induced Obesity in Mice

by Manoja K. Brahma, Peng Xiao, Madalina Popa, Javier Negueruela, Valerie Vandenbempt, Stéphane Demine, Alessandra K. Cardozo and Esteban N. Gurzov

Nutrients 2022, 14(18), 3866; https://doi.org/10.3390/nu14183866 - 18 Sep 2022

Cited by 3 | Viewed by 3004

Abstract

The loss of functional pancreatic β-cell mass is an important hallmark of both type 1 and type 2 diabetes. The RNA-binding protein NOVA1 is expressed in human and rodent pancreatic β-cells. Previous in vitro studies indicated that NOVA1 is necessary for glucose-stimulated insulin [...] Read more.

The loss of functional pancreatic β-cell mass is an important hallmark of both type 1 and type 2 diabetes. The RNA-binding protein NOVA1 is expressed in human and rodent pancreatic β-cells. Previous in vitro studies indicated that NOVA1 is necessary for glucose-stimulated insulin secretion and its deficiency-enhanced cytokine-induced apoptosis. Moreover, Bim, a proapoptotic protein, is differentially spliced and potentiates apoptosis in NOVA1-deficient β-cells in culture. We generated two novel mouse models by Cre-Lox technology lacking Nova1 (βNova1^−/−) or Bim (βBim^−/−) in β-cells. To test the impact of Nova1 or Bim deletion on β-cell function, mice were subjected to multiple low-dose streptozotocin (MLD-STZ)-induced diabetes or high-fat diet-induced insulin resistance. β-cell-specific Nova1 or Bim deficiency failed to affect diabetes development in response to MLD-STZ-induced β-cell dysfunction and death evidenced by unaltered blood glucose levels and pancreatic insulin content. In addition, body composition, glucose and insulin tolerance test, and pancreatic insulin content were indistinguishable between control and βNova1^−/− or βBim^−/− mice on a high fat diet. Thus, Nova1 or Bim deletion in β-cells does not impact on glucose homeostasis or diabetes development in mice. Together, these data argue against an in vivo role for the Nova1-Bim axis in β-cells. Full article

(This article belongs to the Special Issue High Fat Diet with Chronic Diseases)

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13 pages, 2222 KiB

Open AccessArticle

Benefits of Valsartan and Amlodipine in Lipolysis through PU.1 Inhibition in Fructose-Induced Adiposity

by Chu-Lin Chou, Ching-Hao Li and Te-Chao Fang

Nutrients 2022, 14(18), 3759; https://doi.org/10.3390/nu14183759 - 12 Sep 2022

Cited by 2 | Viewed by 2163

Abstract

High fructose intake has been implicated in obesity and metabolic syndrome, which are related to increased cardiovascular mortality. However, few studies have experimentally examined the role of renin–angiotensin system blockers and calcium channel blockers (CCB) in obesity. We investigated the effects of valsartan [...] Read more.

High fructose intake has been implicated in obesity and metabolic syndrome, which are related to increased cardiovascular mortality. However, few studies have experimentally examined the role of renin–angiotensin system blockers and calcium channel blockers (CCB) in obesity. We investigated the effects of valsartan (an angiotensin II receptor blocker) and amlodipine (a CCB) on lipolysis through the potential mechanism of PU.1 inhibition. We observed that high fructose concentrations significantly increased adipose size and triglyceride, monoacylglycerol lipase, adipose triglyceride lipase, and stearoyl-CoA desaturase-1 (SCD1), activating transcription factor 3 and PU.1 levels in adipocytes in vitro. Subsequently, PU.1 inhibitor treatment was able to reduce triglyceride, SCD1, and PU.1 levels. In addition, elevated levels of triglyceride and PU.1, stimulated by a high fructose concentration, decreased with valsartan and amlodipine treatment. Overall, these findings suggest that high fructose concentrations cause triacylglycerol storage in adipocytes through PU.1-mediated activation. Furthermore, valsartan and amlodipine treatment reduced triacylglycerol storage in adipocytes by inhibiting PU.1 activation in high fructose concentrations in vitro. Thus, the benefits of valsartan and amlodipine in lipolysis may be through PU.1 inhibition in fructose-induced adiposity, and PU.1 inhibition might have a potential therapeutic role in lipolysis in fructose-induced obesity. Full article

(This article belongs to the Special Issue High Fat Diet with Chronic Diseases)

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18 pages, 1644 KiB

Open AccessArticle

Combination of Caloric Restriction and a Mixed Training Protocol as an Effective Strategy to Counteract the Deleterious Effects in Trabecular Bone Microarchitecture Caused by a Diet-Induced Obesity in Sprague Dawley Rats

by Elena Nebot, Rosario Martínez, Garyfallia Kapravelou, Cristina Sánchez, Juan Llopis, Pilar Aranda, Jesús M. Porres, María López-Jurado and Peter Pietschmann

Nutrients 2022, 14(18), 3672; https://doi.org/10.3390/nu14183672 - 6 Sep 2022

Cited by 3 | Viewed by 2051

Abstract

The association of obesity with changes in bone mass is not clear. Obese individuals tend to have an increased bone mineral density, but other studies have shown that obesity is a major risk factor for fractures. The mechanisms of bone response during a [...] Read more.

The association of obesity with changes in bone mass is not clear. Obese individuals tend to have an increased bone mineral density, but other studies have shown that obesity is a major risk factor for fractures. The mechanisms of bone response during a weight loss therapy as well as the possible osteoprotective effect of exercise should be analyzed. The aim of this study was to test the effects of a weight-loss program based on the combination of caloric restriction and/or a mixed training protocol on different parameters of bone morphology and functionality in a DIO rat model. Three stages were established over a 21-week period (obesity induction 0–12 w, weight loss intervention 12–15 w, weight maintenance intervention 15–21 w) in 88 male Sprague Dawley rats. Bone microarchitecture, total mineral and elemental composition, and bone metabolism parameters were assessed. Weight loss interventions were associated to healthy changes in body composition, decreasing body fat and increasing lean body mass. On the other hand, obesity was related to a higher content of bone resorption and inflammatory markers, which was decreased by the weight control interventions. Caloric restriction led to marked changes in trabecular microarchitecture, with a significant decrease in total volume but no changes in bone volume (BV). In addition, the intervention diet caused an increase in trabeculae number and a decrease in trabecular spacing. The training protocol increased the pore diameter and reversed the changes in cortical porosity and density of BV induced by the high protein diet at diaphysis level. Regarding the weight-maintenance stage, diminished SMI values indicate the presence of more plate-like spongiosa in sedentary and exercise groups. In conclusion, the lifestyle interventions of caloric restriction and mixed training protocol implemented as weight loss strategies have been effective to counteract some of the deleterious effects caused by a dietary induction of obesity, specifically in trabecular bone morphometric parameters as well as bone mineral content. Full article

(This article belongs to the Special Issue High Fat Diet with Chronic Diseases)

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23 pages, 7114 KiB

Open AccessArticle

Crossbred Sows Fed a Western Diet during Pre-Gestation, Gestation, Lactation, and Post-Lactation Periods Develop Signs of Lean Metabolic Syndrome That Are Partially Attenuated by Spirulina Supplementation

by Rosamaria Lugarà, Simone Renner, Eckhard Wolf, Annette Liesegang, Rupert Bruckmaier and Katrin Giller

Nutrients 2022, 14(17), 3574; https://doi.org/10.3390/nu14173574 - 30 Aug 2022

Cited by 5 | Viewed by 2633

Abstract

Excessive dietary intake of fats and sugars (“Western diet”, WD) is one of the leading causes of obesity. The consumption of the microalga Arthrospira platensis (spirulina, Sp) is increasing due to its presumed health benefits. Both WD and Sp are also consumed by [...] Read more.

Excessive dietary intake of fats and sugars (“Western diet”, WD) is one of the leading causes of obesity. The consumption of the microalga Arthrospira platensis (spirulina, Sp) is increasing due to its presumed health benefits. Both WD and Sp are also consumed by pregnant and breastfeeding women. This study investigated if gestating and lactating domestic pigs are an appropriate model for WD-induced metabolic disturbances similar to those observed in humans and if Sp supplementation may attenuate any of these adverse effects. Pigs were fed a WD high in fat, sugars, and cholesterol or a control diet. Half of the animals per diet group were supplemented with 20 g Sp per day. The WD did not increase body weight or adipose tissue accumulation but led to metabolic impairments such as higher cholesterol concentration in plasma, lower IGF1 plasma levels, and signs of hepatic damage compared to the control group. Spirulina supplementation could not reduce all the metabolic impairments observed in WD-fed animals. These findings indicate limited suitability of gestating and lactating domestic pigs as a model for WD but a certain potential of low-dose Sp supplementation to partially attenuate negative WD effects. Full article

(This article belongs to the Special Issue High Fat Diet with Chronic Diseases)

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18 pages, 3882 KiB

Open AccessArticle

Effects of Oats, Tartary Buckwheat, and Foxtail Millet Supplementation on Lipid Metabolism, Oxido-Inflammatory Responses, Gut Microbiota, and Colonic SCFA Composition in High-Fat Diet Fed Rats

by Yong Wang, Wentao Qi, Xiaoxuan Guo, Ge Song, Shaojie Pang, Wei Fang and Zhenzhen Peng

Nutrients 2022, 14(13), 2760; https://doi.org/10.3390/nu14132760 - 4 Jul 2022

Cited by 35 | Viewed by 4647

Abstract

Coarse cereals rich in polyphenols, dietary fiber, and other functional components exert multiple health benefits. We investigated the effects of cooked oats, tartary buckwheat, and foxtail millet on lipid profile, oxido-inflammatory responses, gut microbiota, and colonic short-chain fatty acids composition in high-fat diet [...] Read more.

Coarse cereals rich in polyphenols, dietary fiber, and other functional components exert multiple health benefits. We investigated the effects of cooked oats, tartary buckwheat, and foxtail millet on lipid profile, oxido-inflammatory responses, gut microbiota, and colonic short-chain fatty acids composition in high-fat diet (HFD) fed rats. Rats were fed with a basal diet, HFD, oats diet (22% oat in HFD), tartary buckwheat diet (22% tartary buckwheat in HFD), and foxtail millet diet (22% foxtail millet in HFD) for 12 weeks. Results demonstrated that oats and tartary buckwheat attenuated oxidative stress and inflammatory responses in serum, and significantly increased the relative abundance of Lactobacillus and Romboutsia in colonic digesta. Spearman’s correlation analysis revealed that the changed bacteria were strongly correlated with oxidative stress and inflammation-related parameters. The concentration of the butyrate level was elevated by 2.16-fold after oats supplementation. In addition, oats and tartary buckwheat significantly downregulated the expression of sterol regulatory element-binding protein 2 and peroxisome proliferator-activated receptors γ in liver tissue. In summary, our results suggested that oats and tartary buckwheat could modulate gut microbiota composition, improve lipid metabolism, and decrease oxidative stress and inflammatory responses in HFD fed rats. The present work could provide scientific evidence for developing coarse cereals-based functional food for preventing hyperlipidemia. Full article

(This article belongs to the Special Issue High Fat Diet with Chronic Diseases)

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15 pages, 2144 KiB

Open AccessArticle

Effects of Fermented Milk Containing Bifidobacterium animalis Subsp. lactis MN-Gup (MN-Gup) and MN-Gup-Based Synbiotics on Obesity Induced by High Fat Diet in Rats

by Chenyuan Wang, Shusen Li, Erna Sun, Ran Xiao, Ran Wang, Yimei Ren, Jingjing He, Qi Zhang and Jing Zhan

Nutrients 2022, 14(13), 2631; https://doi.org/10.3390/nu14132631 - 24 Jun 2022

Cited by 4 | Viewed by 2566

Abstract

Given the probiotic effects previously found in Bifidobacterium animalis subsp. lactis MN-Gup (MN-Gup) and its great application potential in dairy products, this study aimed to investigate the effects of fermented milk containing MN-Gup or MN-Gup-based synbiotics on high fat diet (HFD)-induced obesity in [...] Read more.

Given the probiotic effects previously found in Bifidobacterium animalis subsp. lactis MN-Gup (MN-Gup) and its great application potential in dairy products, this study aimed to investigate the effects of fermented milk containing MN-Gup or MN-Gup-based synbiotics on high fat diet (HFD)-induced obesity in rats. Galacto-oligosaccharides (GOS) and xylo-oligosaccharides (XOS) were selected as the tested prebiotics in MN-Gup-based synbiotics due to their promotion of MN-Gup growth in vitro. After nine weeks of HFD feeding, the obese rats were intervened with fermented milk containing MN-Gup (MN-Gup FM) or its synbiotics (MN-Gup + GOS FM, MN-Gup + XOS FM) for eight weeks. The results showed that the interventions could alleviate HFD-induced body weight gain, epididymal fat deposition, adipocyte hypertrophy, dyslipidemia and inflammation, but GOS and XOS did not exhibit significant synergies with MN-Gup on those alleviations. Furthermore, the interventions could regulate the HFD-affected gut microbiota and microbial metabolites, as shown by the increases in short chain fatty acids (SCFAs) and alterations in obesity-related bile acids (BAs), which may play important roles in the mechanism underlying the alleviation of obesity. This study revealed the probiotic effects of MN-Gup on alleviating obesity and provided the basis for MN-Gup applications in the future. Full article

(This article belongs to the Special Issue High Fat Diet with Chronic Diseases)

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14 pages, 3250 KiB

Open AccessArticle

Swimming Suppresses Cognitive Decline of HFD-Induced Obese Mice through Reversing Hippocampal Inflammation, Insulin Resistance, and BDNF Level

by Hu Zhang, Ji-Ling Liang, Qiu-Yue Wu, Jin-Xiu Li, Ya Liu, Liang-Wen Wu, Jie-Lun Huang, Xiao-Wen Wu, Ming-Hui Wang and Ning Chen

Nutrients 2022, 14(12), 2432; https://doi.org/10.3390/nu14122432 - 11 Jun 2022

Cited by 6 | Viewed by 2782

Abstract

Obesity is an important public health problem nowadays. Long-term obesity can trigger a series of chronic diseases and impair the learning and memory function of the brain. Current studies show that scientific exercise can effectively improve learning and memory capacity, which also can [...] Read more.

Obesity is an important public health problem nowadays. Long-term obesity can trigger a series of chronic diseases and impair the learning and memory function of the brain. Current studies show that scientific exercise can effectively improve learning and memory capacity, which also can provide benefits for obese people. However, the underlying mechanisms for the improvement of cognitive capacity under the status of obesity still need to be further explored. In the present study, the obesity-induced cognition-declined model was established using 4-week-old mice continuously fed with a high-fat diet (HFD) for 12 weeks, and then the model mice were subjected to an 8-week swimming intervention and corresponding evaluation of relevant indicators, including cognitive capacity, inflammation, insulin signal pathway, brain-derived neurotrophic factor (BNDF), and apoptosis, for exploring potential regulatory mechanisms. Compared with the mice fed with regular diets, the obese mice revealed the impairment of cognitive capacity; in contrast, swimming intervention ameliorated the decline in cognitive capacity of obese mice by reducing inflammatory factors, inhibiting the JNK/IRS-1/PI3K/Akt signal pathway, and activating the PGC-1α/BDNF signal pathway, thereby suppressing the apoptosis of neurons. Therefore, swimming may be an important interventional strategy to compensate for obesity-induced cognitive impairment. Full article

(This article belongs to the Special Issue High Fat Diet with Chronic Diseases)

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21 pages, 13138 KiB

Open AccessArticle

Long-Term High-Fat High-Fructose Diet Induces Type 2 Diabetes in Rats through Oxidative Stress

by Yue Zhao, Qing-Yu Wang, Lv-Tao Zeng, Jing-Jing Wang, Zhen Liu, Guo-Qing Fan, Jin Li and Jian-Ping Cai

Nutrients 2022, 14(11), 2181; https://doi.org/10.3390/nu14112181 - 24 May 2022

Cited by 20 | Viewed by 5060

Abstract

Long-term consumption of a Western diet is a major cause of type 2 diabetes mellitus (T2DM). However, the effects of diet on pancreatic structure and function remain unclear. Rats fed a high-fat, high-fructose (HFHF) diet were compared with rats fed a normal diet [...] Read more.

Long-term consumption of a Western diet is a major cause of type 2 diabetes mellitus (T2DM). However, the effects of diet on pancreatic structure and function remain unclear. Rats fed a high-fat, high-fructose (HFHF) diet were compared with rats fed a normal diet for 3 and 18 months. Plasma biochemical parameters and inflammatory factors were used to reflect metabolic profile and inflammatory status. The rats developed metabolic disorders, and the size of the islets in the pancreas increased after 3 months of HFHF treatment but decreased and became irregular after 18 months. Fasting insulin, C-peptide, proinsulin, and intact proinsulin levels were significantly higher in the HFHF group than those in the age-matched controls. Plasmatic oxidative parameters and nucleic acid oxidation markers (8-oxo-Gsn and 8-oxo-dGsn) became elevated before inflammatory factors, suggesting that the HFHF diet increased the degree of oxidative stress before affecting inflammation. Single-cell RNA sequencing also verified that the transcriptional level of oxidoreductase changed differently in islet subpopulations with aging and long-term HFHF diet. We demonstrated that long-term HFHF diet and aging-associated structural and transcriptomic changes that underlie pancreatic islet functional decay is a possible underlying mechanism of T2DM, and our study could provide new insights to prevent the development of diet-induced T2DM. Full article

(This article belongs to the Special Issue High Fat Diet with Chronic Diseases)

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11 pages, 2632 KiB

Open AccessArticle

A High-Fat Diet Induces Muscle Mitochondrial Dysfunction and Impairs Swimming Capacity in Zebrafish: A New Model of Sarcopenic Obesity

by Yun-Yi Zou, Zhang-Lin Chen, Chen-Chen Sun, Dong Yang, Zuo-Qiong Zhou, Qin Xiao, Xi-Yang Peng and Chang-Fa Tang

Nutrients 2022, 14(9), 1975; https://doi.org/10.3390/nu14091975 - 9 May 2022

Cited by 14 | Viewed by 4486

Abstract

Obesity is a highly prevalent disease that can induce metabolic syndrome and is associated with a greater risk of muscular atrophy. Mitochondria play central roles in regulating the physiological metabolism of skeletal muscle; however, whether a decreased mitochondrial function is associated with impaired [...] Read more.

Obesity is a highly prevalent disease that can induce metabolic syndrome and is associated with a greater risk of muscular atrophy. Mitochondria play central roles in regulating the physiological metabolism of skeletal muscle; however, whether a decreased mitochondrial function is associated with impaired muscle function is unclear. In this study, we evaluated the effects of a high-fat diet on muscle mitochondrial function in a zebrafish model of sarcopenic obesity (SOB). In SOB zebrafish, a significant decrease in exercise capacity and skeletal muscle fiber cross-sectional area was detected, accompanied by high expression of the atrophy-related markers Atrogin-1 and muscle RING-finger protein-1. Zebrafish with SOB exhibited inhibition of mitochondrial biogenesis and fatty acid oxidation as well as disruption of mitochondrial fusion and fission in atrophic muscle. Thus, our findings showed that muscle atrophy was associated with SOB-induced mitochondrial dysfunction. Overall, these results showed that the SOB zebrafish model established in this study may provide new insights into the development of therapeutic strategies to manage mitochondria-related muscular atrophy. Full article

(This article belongs to the Special Issue High Fat Diet with Chronic Diseases)

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18 pages, 4560 KiB

Open AccessFeature PaperArticle

Bifidobacterium animalis subsp. lactis A6 Enhances Fatty Acid β-Oxidation of Adipose Tissue to Ameliorate the Development of Obesity in Mice

by Yanxiong Huo, Guoping Zhao, Jinwang Li, Ran Wang, Fazheng Ren, Yixuan Li and Xiaoyu Wang

Nutrients 2022, 14(3), 598; https://doi.org/10.3390/nu14030598 - 29 Jan 2022

Cited by 13 | Viewed by 3147

Abstract

Fatty acid β-oxidation (FAO) is confirmed to be impaired in obesity, especially in adipose tissues. We previously proved that Bifidobacterium animalis subsp. lactis A6 (BAA6) had protective effects against diet-induced obesity. However, whether BAA6 enhances FAO to ameliorate the development of obesity has [...] Read more.

Fatty acid β-oxidation (FAO) is confirmed to be impaired in obesity, especially in adipose tissues. We previously proved that Bifidobacterium animalis subsp. lactis A6 (BAA6) had protective effects against diet-induced obesity. However, whether BAA6 enhances FAO to ameliorate the development of obesity has not been explored. After being fed with high-fat diet (HFD) for 9 weeks, male C57BL/6J mice were fed HFD or BAA6 for 8 weeks. In vitro study was carried out using 3T3-L1 adipocytes to determine the effect of BAA6 culture supernatant (BAA6-CM). Here, we showed that administration of BAA6 to mice fed with HFD decreased body weight gain (by 5.03 g) and significantly up-regulated FAO in epididymal adipose tissues. In parallel, FAO in 3T3-L1 cells was increased after BAA6-CM treatment. Acetate was identified as a constituent of BAA6-CM that showed a similar effect to BAA6-CM. Furthermore, acetate treatment activated the GPR43-PPARα signaling, thereby promoting FAO in 3T3-L1 cells. The levels of acetate were also elevated in serum and feces (by 1.92- and 2.27-fold) of HFD-fed mice following BAA6 administration. The expression levels of GPR43 and PPARα were increased by 55.45% and 69.84% after BAA6 supplement in the epididymal fat of mice. Together, these data reveal that BAA6 promotes FAO of adipose tissues through the GPR43-PPARα signaling, mainly by increasing acetate levels, leading to alleviating the development of obesity. Full article

(This article belongs to the Special Issue High Fat Diet with Chronic Diseases)

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Review

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17 pages, 2069 KiB

Open AccessReview

The Roles of Lipid Metabolism in the Pathogenesis of Chronic Diseases in the Elderly

by Rui Song, Mengxiao Hu, Xiyu Qin, Lili Qiu, Pengjie Wang, Xiaoxu Zhang, Rong Liu and Xiaoyu Wang

Nutrients 2023, 15(15), 3433; https://doi.org/10.3390/nu15153433 - 3 Aug 2023

Cited by 9 | Viewed by 5291

Abstract

Lipid metabolism plays crucial roles in cellular processes such as hormone synthesis, energy production, and fat storage. Older adults are at risk of the dysregulation of lipid metabolism, which is associated with progressive declines in the physiological function of various organs. With advancing [...] Read more.

Lipid metabolism plays crucial roles in cellular processes such as hormone synthesis, energy production, and fat storage. Older adults are at risk of the dysregulation of lipid metabolism, which is associated with progressive declines in the physiological function of various organs. With advancing age, digestion and absorption commonly change, thereby resulting in decreased nutrient uptake. However, in the elderly population, the accumulation of excess fat becomes more pronounced due to a decline in the body’s capacity to utilize lipids effectively. This is characterized by enhanced adipocyte synthesis and reduced breakdown, along with diminished peripheral tissue utilization capacity. Excessive lipid accumulation in the body, which manifests as hyperlipidemia and accumulated visceral fat, is linked to several chronic lipid-related diseases, including cardiovascular disease, type 2 diabetes, obesity, and nonalcoholic fatty liver disease. This review provides a summary of the altered lipid metabolism during aging, including lipid digestion, absorption, anabolism, and catabolism, as well as their associations with age-related chronic diseases, which aids in developing nutritional interventions for older adults to prevent or alleviate age-related chronic diseases. Full article

(This article belongs to the Special Issue High Fat Diet with Chronic Diseases)

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20 pages, 413 KiB

Open AccessReview

The Role of Gut Microbiota in High-Fat-Diet-Induced Diabetes: Lessons from Animal Models and Humans

by Yue Qi and Xiaofei Wang

Nutrients 2023, 15(4), 922; https://doi.org/10.3390/nu15040922 - 12 Feb 2023

Cited by 11 | Viewed by 4446

Abstract

The number of diabetes mellitus patients is increasing rapidly worldwide. Diet and nutrition are strongly believed to play a significant role in the development of diabetes mellitus. However, the specific dietary factors and detailed mechanisms of its development have not been clearly elucidated. [...] Read more.

The number of diabetes mellitus patients is increasing rapidly worldwide. Diet and nutrition are strongly believed to play a significant role in the development of diabetes mellitus. However, the specific dietary factors and detailed mechanisms of its development have not been clearly elucidated. Increasing evidence indicates the intestinal microbiota is becoming abundantly apparent in the progression and prevention of insulin resistance in diabetes. Differences in gut microbiota composition, particularly butyrate-producing bacteria, have been observed in preclinical animal models as well as human patients compared to healthy controls. Gut microbiota dysbiosis may disrupt intestinal barrier functions and alter host metabolic pathways, directly or indirectly relating to insulin resistance. In this article, we focus on dietary fat, diabetes, and gut microbiome characterization. The promising probiotic and prebiotic approaches to diabetes, by favorably modifying the composition of the gut microbial community, warrant further investigation through well-designed human clinical studies. Full article

(This article belongs to the Special Issue High Fat Diet with Chronic Diseases)

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