Diet Control Group Research Articles

Solanum nigrum show anti-obesity effects on high-fat diet-fed Sprague Dawley rats in a randomized study

Solanum nigrum also known as black night shade biosynthesizes various bioactive compounds which have various pharmacological activities including treating cardiovascular diseases, diabetes type 2 among others. To assess the anti-obesity effects of Solanum nigrum using high-fat-fed diet rats, Sprague Dawley male rats (n = 35) of weights 160–180 g were assigned randomly into seven groups comprising n = 5 rats each. Each group was fed for 11 weeks as follows: normal group (normal chow rat feed); high-fat diet control (HFD); HFD and standard drug (Orlistat 30 mg/kg bw); HFD and methanolic extract 150 mg/kgbw; HFD and methanolic extract 300 mg/kgbw; HFD and dichloromethane extract 150 mg/kgbw; HFD and dichloromethane extract 300 mg/kgbw. Body mass index and food intake were monitored per week and an oral glucose tolerance test was measured in weeks 5 and 10. Lipid profiles, liver function tests, adipose tissue, liver weights, and phytochemical analysis of Solanum nigrum were later carried out. ResultsHigh-fat diet control group rats exhibited a significant increase in body mass index (BMI) while rats administered with leaf extracts of Solanum nigrum showed a reduction in BMI. Both low dose of dichloromethane (150 mg/kgbw) and high dose of methanol extracts (300 mg/kgbw) showed a better reduction in BMI than the other treatment groups. A significant decrease (p <0.05) on low-density lipoprotein-cholesterol, triglycerides and cholesterol was observed among the rats administered with Solanum nigrum extracts compared to those of HFD control. Moreover, the HFD control group significantly increased liver and adipose tissue weights compared to other treatments groups (p<0.05). Solanum nigrum also decreased glycemic levels and normalized the hepatic enzymes of HFD control. However, food intake among the groups showed no significant difference (p>0.05). Qualitative analysis of Solanum nigrum leave extracts indicated the presence of various bioactive compounds associated with anti-obesity. ConclusionThese results validate the use of Solanum nigrum in controlling obesity.

Ketogenic diet alleviates cognitive dysfunction and neuroinflammation in APP/PS1 mice via the Nrf2/HO-1 and NF-κB signaling pathways.

Alzheimer's disease is a progressive neurological disorder characterized by cognitive decline and chronic inflammation within the brain. The ketogenic diet, a widely recognized therapeutic intervention for refractory epilepsy, has recently been proposed as a potential treatment for a variety of neurological diseases, including Alzheimer's disease. However, the efficacy of ketogenic diet in treating Alzheimer's disease and the underlying mechanism remains unclear. The current investigation aimed to explore the effect of ketogenic diet on cognitive function and the underlying biological mechanisms in a mouse model of Alzheimer's disease. Male amyloid precursor protein/presenilin 1 (APP/PS1) mice were randomly assigned to either a ketogenic diet or control diet group, and received their respective diets for a duration of 3 months. The findings show that ketogenic diet administration enhanced cognitive function, attenuated amyloid plaque formation and proinflammatory cytokine levels in APP/PS1 mice, and augmented the nuclear factor-erythroid 2-p45 derived factor 2/heme oxygenase-1 signaling pathway while suppressing the nuclear factor-kappa B pathway. Collectively, these data suggest that ketogenic diet may have a therapeutic potential in treating Alzheimer's disease by ameliorating the neurotoxicity associated with Aβ-induced inflammation. This study highlights the urgent need for further research into the use of ketogenic diet as a potential therapy for Alzheimer's disease.

Eryngium billardieri extract affects cardiac gene expression of master regulators of cardiomyaopathy in rats with high fatdiet-induced insulin resistance

For years, numerous studies have focused on identifying approaches to increase insulin sensitivity by modifying the signaling factors. In the present study, we examined the effects of Eryngium billardieri extract, as an anti-diabetic herbal medication, on the heart mRNA level of Akt serine/threonine kinase (Akt), mechanistic target of rapamycin kinase (mTOR), peroxisome proliferator-activated receptor gamma (PPARγ), and Forkhead box o1 (Foxo1) in rats with high-fat diet (HFD)-induced insulin resistance (IR). We also assessed the anti-diabetic effects of E.billardieri extract in rats with insulin resistance. Twenty-seven male Wistar rats were divided into two groups. Nine rats were fed a normal diet (control group), and 18 rats were fed an HFD for 13 weeks (HFD group). To confirm the induction of insulin resistance, the oral glucose tolerance test (OGTT) was performed and homeostatic model assessment for insulin resistance (HOMA-IR) was calculated. Then rats with IR were randomly divided into the following groups: the HFD group, which continued an HFD, and the group treated with E.billardieri extract, which received the extract at a concentration of 50mg/kg for 30 days. On the 30th day, the animals were sacrificed and serum samples were collected for biochemistry analyses. Furthermore, the expression of Akt, mTOR, PPARγ, and Foxo1 was measured in heart tissue using the real-time polymerase chain reaction (PCR) method. Real-time PCR analyses revealed that an HFD can significantly decrease the expression level of Akt, mTOR, and PPARγ in the heart tissue. However, an HFD significantly increased the expression level of Foxo1 in the HFD group compared to the control group (P<0.05). In addition, our data showed that the administration of E. billardieri extract significantly enhanced the mRNA levels of Akt, PPARγ, and mTOR in the heart tissue compared to the HFD group (P<0.05), while it significantly decreased the Foxo1 mRNA levels (P<0.01). Given that Akt, mTOR, PPARγ, and Foxo1 are critical factors in insulin resistance, the present study suggests that E.billardieri could probably be used as an alternative treatment for IR as a major feature of metabolic syndrome.

Effects of different doses of exercise and diet-induced weight loss on beta-cell function in type 2 diabetes (DOSE-EX): a randomized clinical trial

Diet-induced weight loss is associated with improved beta-cell function in people with type 2 diabetes (T2D) with remaining secretory capacity. It is unknown if adding exercise to diet-induced weight loss improves beta-cell function and if exercise volume is important for improving beta-cell function in this context. Here, we carried out a four-armed randomized trial with a total of 82 persons (35% females, mean age (s.d.) of 58.2 years (9.8)) with newly diagnosed T2D (<7 years). Participants were randomly allocated to standard care (n = 20), calorie restriction (25% energy reduction; n = 21), calorie restriction and exercise three times per week (n = 20), or calorie restriction and exercise six times per week (n = 21) for 16 weeks. The primary outcome was beta-cell function as indicated by the late-phase disposition index (insulin secretion multiplied by insulin sensitivity) at steady-state hyperglycemia during a hyperglycemic clamp. Secondary outcomes included glucose-stimulated insulin secretion and sensitivity as well as the disposition, insulin sensitivity, and secretion indices derived from a liquid mixed meal tolerance test. We show that the late-phase disposition index during the clamp increases more in all three intervention groups than in standard care (diet control group, 58%; 95% confidence interval (CI), 16 to 116; moderate exercise dose group, 105%; 95% CI, 49 to 182; high exercise dose group, 137%; 95% CI, 73 to 225) and follows a linear dose–response relationship (P > 0.001 for trend). We report three serious adverse events (two in the control group and one in the diet control group), as well as adverse events in two participants in the diet control group, and five participants each in the moderate and high exercise dose groups. Overall, adding an exercise intervention to diet-induced weight loss improves glucose-stimulated beta-cell function in people with newly diagnosed T2D in an exercise dose-dependent manner (NCT03769883).

Effect of increasing dietary methionine-to-lysine ratio during early gestation on fetal development and piglet birth weight

It was hypothesized that increasing dietary methionine (Met) for sows in early gestation would have a positive effect on fetal and placental growth and development, thereby also increasing the birth weight of piglets. The objective of the study was to investigate the effect of increasing the total dietary methionine-to-lysine ratio (Met:Lys) from 0.29 (Control diet) to 0.41 (Met diet) from mating to day 50 of gestation. A total of 349 multiparous sows were allocated to either the Control or Met diet group. The sows’ backfat thickness was measured pre-farrowing, post-farrowing, and at weaning in the previous cycle and on days 14, 50 and 112 of gestation in the current cycle. On day 50, three Control and six Met sows were slaughtered. In 116 litters, piglets were weighed and measured individually at farrowing. The dietary treatment did not affect the sows’ backfat thickness before or during gestation (P > 0.05). The number of liveborn and stillborn piglets at farrowing were similar in both groups (P > 0.05) and no differences in average piglet birth weight, total litter weight at birth or within-litter variation in birth weight (P > 0.05) were observed. In conclusion, increasing the dietary Met:Lys ratio for sows in early gestation had no effect on piglet birth weight.

Assessing the hepatoprotective effects of hesperidin on liver-associated disorders in albino rats with experimentally induced obesity and type II diabetes: A histological and biochemical study

IntroductionHesperidin (HSP) has multiple beneficial effects in verities of clinical situations including type 2 diabetes mellitus (T2DM). Aim: Determination of curative effects of HSP on the liver in T2DM rats through biochemical and histopathological studies. Methods: Animals. Fifty rats were enrolled. 10 rats were fed a normal diet (control group), and the remaining 40 rats received a high-fat diet (HFD) for 8 weeks. The HFD-fed rats were grouped into Group II: 10 rats, and Group III: 10 rats received HSP 100 mg/kg. Group IV: 10 rats received a single dose of streptozotocin (STZ), 30 mg/kg, and Group V: 10 rats received STZ and HSP. Body weight, Blood glucose, insulin level, liver enzymes, lipid profile, oxidative stress, TNF-α, NF-κB, and liver biopsy were estimated. Results: there is improvement in the histological profile of the steatosis in HFD-fed rats treated with HSP either in group III or in group V (received STZ) along with amelioration in blood glucose, insulin, liver enzymes, lipid profile, oxidative profile, TNF-α, and NF-κB. Conclusion: HSP in this STZ model revealed an improvement in steatosis, biochemical markers, and histologic findings. By studying these factors, we expected to identify the prospective targets for intervention that could help improve outcomes for individuals with obesity and diabetes-related liver diseases.

Fibroadipogenic progenitor-derived Gdf10 regulates neuromuscular junction and fat content in tongue muscles

Obstructive sleep apnea (OSA) is the most prevalent sleep disorder globally 4.5% in men and 2.5% in women. OSA increases the risk of more severe diseases such as heart attack, high blood pressure, type 2 diabetes, obesity, mild cognitive impairment, and depression. The known craniofacial anatomical changes leading to OSA are relaxed muscles and/or enlarged soft tissues by fat infiltration in the soft palate, pharynx, and particularly tongue, which blocks the upper airway during sleep. Although obesity is one of the main causes to induce OSA, the underlying mechanism of those changes has not been researched. The objective of our study is to understand the mechanism leading to those craniofacial changes that generate foundations to develop potential therapeutics for OSA. We hypothesize that high-fat diet-induced obesity regulates the fibroadipogenic progenitors, which are critical for neuromuscular interaction and is mainly responsible for increased fat content in skeletal muscles. To test this hypothesis, we used a mouse model fed with a high-fat diet to induce obesity or a normal diet (control group) for 6 months. Then we isolated tongue muscles for histology analysis, such as muscle size, neuromuscular junction integrity, and adipocyte content.We found that a high-fat diet leaded adipocyte hypertrophy and reduced intact neuromuscular junction in tongue muscles. To investigate the role of fibroadipogenic progenitors for tongue phenotypes by a high-fat diet, we isolated fibroadipogenic progenitor cells to measure transcript levels of Gdf10, also known as Bmp3b, since fibroadipogenic progenitor-derived Gdf10 has been known to stabilize Schwann cells for neuromuscular integrity in muscles. The role of Gdf10 has been suggested to protect from obesity by limiting adipocyte hypertrophy. Using single-cell RNA sequencing analysis, Gdf10 is specifically expressed in fibroadipogenic progenitors but not adipocyte or Schwann cells. We found that Gdf10 transcript levels are significantly reduced by a high-fat diet in tongue fibroadipose progenitors. Taken together, the reduced Gdf10 of fibroadipogenic progenitors by a high-fat diet reduces neuromuscular integrity but induces fat infiltration in tongue muscles in a paracrine manner. Therefore, targeting to increase Gdf10 expression is a potential therapeutic to reduce OSA by maintaining healthy tongue muscle. NIH R01AR071397 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

The Protective Effect of Zinc on Salt Induced Histological Changes in Femur of Sprague Dawley Rats-Data Driven Approach

Background: Osteoporosis, a degenerative skeletal illness, is a widespread medical issue that can affect a person's way of life. Aim: To evaluate how salt played a protective role in the Sprague Dawley rats' femur's microscopic alterations. Study Design: Random control trial Methodology: The study used 30 female, Sprague Dawley rats aged between 0 and 12 weeks. Three groups of the animals were randomly chosen. For eight weeks, group B rodents received a high salt diet supplemented with zinc (50 mg/kg/day), while group A rats were administered a high salt diet (8% NaCl). The control group's diet was left unaltered. The left femora of the rats were excised during dissection. There was a decalcification process. To quantify the cortical bone, tissue from the mid-shaft of the femur was taken. To acquire five micrometer (m) sections, processing was done. Hematoxylin and Eosin (H&amp;E) was used to stain tissues as a histological parameter. Each group was compared to the others. Statistical analysis: MATLAB was used to conduct the data analysis. Mean+ S.D. was used to express quantitative data. For group comparisons, a 2-sample t-test was used. Statistical significance was defined as p 0.05. Results: Group A of the experimental study had a considerably smaller area of cortical bone from the mid shaft of the femur. When compared to group A, the experimental zinc-administered group B showed statistically significant improvements. Practical Implication: Osteoporosis is a multifactorial disease and numerous micro/macro nutrients and dietary components can influence bone health including high salt intake. Zinc plays a pivotal role in maintenance and growth of skeletal system and its deficiency results in growth failure, epidermal, gastrointestinal, central nervous, immune, skeletal, and reproductive systems disorders so present study was planned. Conclusion: A diet high in salt caused bone loss due to a reduction in the cortex's surface area. By promoting osteoblast activity and preventing bone-resorbing cells, zinc is useful in reducing the negative effects of salt on bones. Keywords: Cortex, Femur, Osteaoprosis, Salt and Zinc

CONSUMPTION OF BROCCOLI SPROUTS INCREASED THE ACTIVITY OF GLUTATHIONE-DEPENDENT ANTIOXIDANT ENZYMES IN MURINE LIVER

Aim. The purpose of this work was to investigate effects of the consumption of broccoli sprouts on the activity of antioxidant defense enzymes in the liver of. GPx isoforms. After photo fixation of gels, we determined activity of each isoform densitometrically using ImageJ software. Results were statistically analyzed by ANOVA followed by post-hoc Tukey's test. Data are presented as mean±SEM. Methods. Frozen tissue was homozeniged in lysis buffer, centrifuged and resulted supernatants were used for analysis. Activities of enzymes were determined by using electrophoresis in polyacrylamide gel. After electrophoresis we conducted dyeing of separate gels for detection of superoxide dismutase (SOD), glutathione-S-transferase (GST) or glutathione peroxidase (GPx) isoforms. After photo fixation of gels, we determined activity of each isoform densitometrically using ImageJ software. Results were statistically analyzed by ANOVA followed by post-hoc Tukey's test. Data are presented as mean±SEM. Results. In the hepatic tissue of all four groups of mice, two isoforms of SOD (SOD1 and SOD2) were detected in gels. The intensity of the bands of both isoforms was not significantly different between groups. Three isoforms of GST (GST1, GST2, GST3) were detected in the liver samples. The activity of GST1 did not significantly differ between the experimental groups. Activities of GST2 and GST3 forms were significantly higher in the group “Broccoli” compared to Control and Cafeteria Diet groups. We identified three isoforms of glutathione peroxidase (GPx1, GPx2, GPx3) in liver samples. The activity of GPx isoform 1 was not significantly different between the experimental groups. The activity of GPx2 was significantly higher in the group of mice that consumed Broccoli and Cafeteria Diet + Broccoli compared to Control. GPx2 activity was significantly higher in the Broccoli group compared to the Cafeteria Diet group. Activity of GPx3 was significantly higher in the Broccoli group compared to the Control and Cafeteria Diet group. Conclusions. Cafeteria diet did not significantly affect the activity of SOD isoforms, but led to redistribution of in the activity of GST and GPx isoforms in murine liver. Feeding with broccoli spouts significantly increased the activity of 2 and 3 isoforms of GST and GPx in murine liver compared to values in control mice and mice fed with cafeteria diet. Combination of Broccoli + Cafereria diet had small activating effects on antioxidant enzyme acivity, compared with cafeteria diet.

Pyrroloquinoline quinone promotes growth and intestinal health and alleviates tris(1,3-dichloro-2-propyl) phosphate-induced hepatic oxidative stress in zebrafish

Pyrroloquinoline quinone (PQQ) is a newly discovered redox coenzyme possessing multiple biological activities, whose role in nutritional and physiological regulation in fish remains elusive. In this study, we explored how the dietary PQQ influenced the growth, intestinal health and oxidative stress of liver triggered by tris(1,3-dichloro-2-propyl) phosphate (TDCPP) in zebrafish, which was accomplished through a long-term feeding trial (experiment 1) and a short-term stress trial (experiment 2). In experiment 1, two-month-old zebrafish were fed experimental diets either involving 0.4 mg/kg (low PQQ, LP) or 1.6 mg/kg PQQ·Na2 (high PQQ, HP), or a basal diet (CNT) for four weeks. It showed that compared to the zebrafish in the CNT group, those in the LP and HP groups exhibited remarkably improved growth performance, whose feed conversion ratio was lower, while specific growth rate and weight gain rate higher. No significant intestinal pathological symptoms were found among groups, albeit the prominently increased villus height of zebrafish in LP and HP groups than the CNT zebrafish. Dietary PQQ led to great phylum- and genus-level modulation of intestinal microflora and made it more balanced. In experiment 2, four-month-old adult zebrafish were fed a basal diet (control group), a basal diet under TDCPP exposure (TDCPP group), a HP diet under TDCPP exposure (TDCPP+PQQ group), or a HP diet (PQQ group) for one week. After the stress trial, significant intrahepatic pathological symptoms were found in the TDCPP group, while TDCPP+PQQ and PQQ groups exhibited no significant stress injury. Further analysis implied that dietary PQQ significantly alleviated the TDCPP-triggered intrahepatic oxidative stress of zebrafish by elevating the antioxidation-related gene levels, potentiating the antioxidant enzyme activities and maintaining appropriate level of apoptosis. Taken together, this study suggested that PQQ could improve growth performance and intestinal health and alleviate the TDCPP-induced liver oxidative stress in zebrafish.

Effect of dietary supplementation of Spirulina platensis powder on performance, some serum biochemistry, digestive enzymes, microbial content, antioxidant parameters and immune responses of growing Japanese quail

This study was performed to examine the influences of Spirulina platensis powder (SPP) on growth performance, physiological status, blood biochemistry, and intestinal microbial population in quail. 240-10-days old Japanese quail chicks were distributed into five groups. Each group had four replicate pens with 12 birds each. The first group received a basal diet (control group). Groups from two to five received the basal diet with SPP at levels of 1.5, 3.0, 4.5, and 6.0% as dietary ingredients, respectively. Results clarified significantly higher live body weight and body weight gain (p < 0.001) with significant enhancements (p < 0.001) in feed conversion values for groups that received SPP levels, especially 4.5% compared with the control and other groups. Birds fed on a diet containing SPP had significantly higher amylase, trypsin and lipase levels (p < 0.001) than the control. Intestinal Lactobacillus sp. was significantly increased, and Escherichia coli and Salamonella populations were significantly decreased by dietary SPP levels (p < 0.001). Liver function, total lipid profile, antioxidant parameters and immune response were significantly affected by SPP levels compared with the control (p < 0.001). In conclusion, the inclusion of SPP until 4.5% in quail diets could improve the growth performance, intestinal microbial population and serum biochemical constituents of growing quail.

Postweaning cafeteria diet induces a short-term metabolic disfunction and a differential vulnerability to develop anxiety-like and depressive-like behaviors in male but not female rats.

Children and adolescents are high consumers of Western diets (rich in fat and sugars), which is a risk factor for overweight and obesity. Moreover, the presence of anxiety and depression among this population has increased significantly. This study explores in young postweaning rats the association between Western diet consumption and the development of metabolic and behavioral disturbances. At postnatal day (PN) 24,Wistarratsof both sexes were weaned and assigned to a control or cafeteria diet (CAF) group. After short-term exposure, a group of rats was euthanized at PN31 to obtain abdominal fat pads and blood samples. Another group of rats was tested in the open-field test, splash test, anhedonia test, and social play across 11days (PN32-42). The CAF groups exhibited a significantly high level of body fat, serum glucose, triglycerides, leptin, and HOMA index when compared to the control groups. Only CAF males exhibited anxiety-like and depression-like behavior. Present results indicate that postweaning short-term exposure to a CAF diet has immediate detrimental effects on metabolism in both sexes. However, only CAF males showed mood disturbances. This study provides evidence that a CAF diet exerts immediate effects on behavior and metabolism in the postweaning period and that sexes present differential vulnerability.

OBESITY IMPAIRS ENTHESIS HEALING AFTER ROTATOR CUFF REPAIR IN A RAT MODEL

Obesity is associated with poor outcomes and increased risk of failure after rotator cuff (RC) repair surgery. The effect of diet-induced obesity (DIO) on enthesis healing has not been well characterised and whether its effects can be reversed with dietary intervention is unknown. We hypothesised that DIO would result in inferior enthesis healing in a rat model of RC repair and that dietary intervention in the peri-operative period would improve enthesis healing.A total of 78 male Sprague-Dawley rats were divided into three weight-matched groups from weaning and fed either: control diet (CD), high-fat diet (HFD), or HFD until surgery, then CD thereafter (HF-CD). After 12 weeks the left supraspinatus tendon was detached, followed by immediate surgical repair. At 2 and 12 weeks post-surgery, animals were cullers and RCs harvested for biomechanical and histological evaluation. Body composition and metabolic markers were assessed via DEXA and plasma analyses, respectively.DIO was established in the HFD and HF-CD groups prior to surgery, and subsequently reversed in the HF-CD group after surgery. At 12 weeks post-surgery, plasma leptin concentrations were higher in the HFD group compared to the CD group (5.28 vs. 2.91ng/ml, P=0.003). Histologically, the appearance of the repaired entheses was poorer in both the HFD and HF-CD compared to the CD group at 12 weeks (overall histological score 6.20 (P=0.008), 4.98 (P=0.001) and 8.68 out of 15, respectively). The repaired entheses in the HF-CD group had significantly lower (26.4 N, P=0.028) load-at-failure 12 weeks post-surgery compared to the CD group (34.4 N); while the HFD group was low, but not significantly different (28.1 N, P=0.096). Body mass at the time of surgery, plasma leptin and body fat percentage were negatively correlated with histological scores and plasma leptin with load-at-failure 12 weeks post-surgery.DIO impaired enthesis healing in this rat RC repair model, with inferior biomechanical and histological outcomes. Restoring normal weight with dietary change after surgery did not improve healing outcomes. Exploring interventions that improve the metabolic state of obese patients and counselling patients appropriately about their modest expectations after repair should be considered.

Effects of Long-Term Aerobic Exercise on Perivascular Adipose Tissue Function and Akt/eNOS/NO Pathway in Obese Rats

BackgroundPerivascular adipose tissue (PVAT) in obesity critically contributes to vascular dysfunction, which might be restored by long-term exercise. Protein kinase B/nitric oxide synthase/nitric oxide (Akt/eNOS/NO) down-regulation within PVAT might be involved in the impaired anti-contractile function of arteries. Therefore, the present study evaluated the effect of long-term aerobic exercise on PVAT function and the potential regulator during this process.MethodsMale Sprague Dawley rats were divided into normal diet control group (NC), normal diet exercise group (NE), high-fat diet control group (HC), and high-fat diet exercise group (HE) (n = 12 in each group). Upon the establishment of obesity (20 weeks of high-fat diet), exercise program was performed on a treadmill for 17 weeks. After the intervention, circulating biomarkers and PVAT morphology were evaluated. Vascular contraction and relaxation were determined with or without PVAT. Production of NO and the phosphorylations of Akt (Ser473) and eNOS (Ser1177) within PVAT were quantified.ResultsMetabolic abnormalities, systemic inflammation, and circulating adipokines in obesity were significantly restored by long-term aerobic exercise (P < 0.05). The anti-contractile effect of PVAT was significantly enhanced by exercise in obese rats (P < 0.05), which was accompanied by a significant reduction in the PVAT mass and lipid droplet area (P < 0.05). Furthermore, the production of NO was significantly increased, and phosphorylation levels of Akt (Ser473) and eNOS (Ser1177) were also significantly promoted in PVAT by long-term aerobic exercise (P < 0.05).ConclusionLong-term aerobic exercise training restored PVAT morphology and anti-contractile function in obese rats, and enhanced the activation of the Akt/eNOS/NO signaling pathway in PVAT.

High-fat diet and oral infection induced type 2 diabetes and obesity development under different genetic backgrounds.

Type 2 diabetes (T2D) is an adult-onset and obese form of diabetes caused by an interplay between genetic, epigenetic, and environmental components. Here, we have assessed a cohort of 11 genetically different collaborative cross (CC) mouse lines comprised of both sexes for T2D and obesity developments in response to oral infection and high-fat diet (HFD) challenges. Mice were fed with either the HFD or the standard chow diet (control group) for 12 weeks starting at the age of 8 weeks. At week 5 of the experiment, half of the mice of each diet group were infected with Porphyromonas gingivalis and Fusobacterium nucleatum bacteria strains. Throughout the 12-week experimental period, body weight (BW) was recorded biweekly, and intraperitoneal glucose tolerance tests were performed at weeks 6 and 12 of the experiment to evaluate the glucose tolerance status of mice. Statistical analysis has shown the significance of phenotypic variations between the CC lines, which have different genetic backgrounds and sex effects in different experimental groups. The heritability of the studied phenotypes was estimated and ranged between 0.45 and 0.85. We applied machine learning methods to make an early call for T2D and its prognosis. The results showed that classification with random forest could reach the highest accuracy classification(ACC=0.91) when all the attributes were used. Using sex, diet, infection status, initial BW, and area under the curve (AUC) at week 6, we could classify the final phenotypes/outcomes at the end stage of the experiment (at 12 weeks).

Blueberry extract alleviated lipopolysaccharide-induced inflammation responses in mice through activating the FXR/TGR5 signaling pathway and regulating gut microbiota.

Blueberry extract (BE) is rich in phenols, especially anthocyanins. Anthocyanins regulate the inflammatory response in mice and may be related to gut microbiota and bile acid receptors. The aim of the present study was to explore the effects of BE on the inflammatory response by regulating gut microbiota and bile acid receptors in mice administered Escherichia coli lipopolysaccharide (LPS). Thirty male KM mice were randomly divided into three groups: CON (control diet) group; LPS (LPS stimulation) group; and LPS + BE (LPS stimulation, 5% BE intervention) group. our results showed that, compared with the LPS group, the addition of BE decreased the level of inflammatory factors in serum and tissues, inhibited the TLR4/MyD88 signaling pathway, protected the intestinal barrier and activated FXR/TGR5, which was related to gut microbiota (especially Akkermansia). The active component (e.g., cyanidin 3-O-glucoside, C3G) in BE may be an important factor in regulating gut microbiota. BE alleviated the inflammatory response mainly by activating bile acid receptor expression and regulating the gut microbiota; this effect may be related to the composition of bioactive substances in BE. © 2023 Society of Chemical Industry.

The Fatty Acid and Mineral Composition of Cobb 500 Broiler Meat Influenced by the Nettle (Urtica dioica) Dietary Supplementation, Broiler Gender and Muscle Portion

The objective of the present trial was to evaluate the effects of nettle leaves (Urtica dioica) supplementation, broiler gender and muscle portion on meat fatty acid and mineral profiles. Prior to the trial, a total of 600 one-day-old Cobb 500 broiler chickens of both genders, equally, were randomly divided into three groups: a basal diet (control group) and a basal diet supplemented in the last two weeks of fattening with fresh nettle leaves (30 g/kg diet) or with oven dry nettle leaves (5 g/kg diet). After reaching 42 days of age, twenty birds per diet group were randomly selected (four birds per box, both genders equally) and slaughtered, and breasts and drumsticks were collected for analysis. The dry nettle supplementation increased the MUFA and lowered the PUFA, n-6 and n-6/n-3 ratio, mainly in female broilers (p &lt; 0.05). Drumsticks had higher MUFA and PUFA and lower SFA and n-6/n-3 ratio compared to breast meat (p &lt; 0.05). The addition of nettle to broiler diet increased Fe, Zn and Se and decreased Ca levels, mainly in drumsticks (p &lt; 0.05). Furthermore, drumstick meat had more elements with proven health benefits, such as Fe, Zn, Ca and Mn, than breast meat. This study suggests that feeding Cobb 500 broilers with the addition of nettle leaves can significantly change meat fatty acid and mineral composition, but this effect differed between gender and portion.

Time-restricted feeding's effect on overweight and obese patients with chronic kidney disease stages 3-4: A prospective non-randomized control pilot study.

Time-restricted feeding (TRF) has become a popular weight loss method in recent years. It is widely used in the nutritional treatment of normal obese people and obese people with chronic diseases such as diabetes mellitus and hypertension, and has shown many benefits. However, most TRF studies have excluded chronic kidney disease (CKD) patients, resulting in a lack of sufficient evidence-based practice for the efficacy and safety of TRF therapy for CKD. Therefore, we explore the efficacy and safety of TRF in overweight and obese patients with moderate-to-severe stage CKD through this pilot study, and observe patient compliance to assess the feasibility of the therapy. This is a prospective, non-randomized controlled short-term clinical trial. We recruited overweight and obese patients with CKD stages 3-4 from an outpatient clinic and assigned them to either a TRF group or a control diet (CD) group according to their preferences. Changes in renal function, other biochemical data, anthropometric parameters, gut microbiota, and adverse events were measured before the intervention and after 12 weeks. The change in estimated glomerular filtration rate (eGFR) before and after intervention in the TRF group (Δ = 3.1 ± 5.3 ml/min/1.73m2) showed significant improvement compared with the CD group (Δ = -0.8 ± 4.4 ml/min/1.73m2). Furthermore, the TRF group had a significant decrease in uric acid (Δ = -70.8 ± 124.2 μmol/L), but an increase in total protein (Δ = 1.7 ± 2.5 g/L), while the changes were inconsistent for inflammatory factors. In addition, the TRF group showed a significant decrease in body weight (Δ = -2.8 ± 2.9kg) compared to the CD group, and body composition indicated the same decrease in body fat mass, fat free mass and body water. Additionally, TRF shifted the gut microbiota in a positive direction. Preliminary studies suggest that overweight and obese patients with moderate-to-severe CKD with weight loss needs, and who were under strict medical supervision by healthcare professionals, performed TRF with good compliance. They did so without apparent adverse events, and showed efficacy in protecting renal function. These results may be due to changes in body composition and alterations in gut microbiota.

Effects of dietary Cetobacterium somerae on the intestinal health, immune parameters and resistance against Nocardia seriolae of largemouth bass, Micropterus salmoides

Largemouth bass (Micropterus salmoides), one of the most important freshwater commercial fish species has been widely cultivated in China. In recent years, the nocardiosis caused by Nocardia seriolae has greatly damaged the M. salmoides industry and there is no effective treatment at present. Currently, Cetobacterium somerae, the predominant bacteria in the gut of many freshwater fishes has been reported to be associated with fish health. However, whether the native C. somerae could protect the host from N. seriolae is unclear. In this study, M. salmoides were fed with three different diets, including control diet (CD), low C. somerae diet (106 CFU/g as LD) and high C. somerae diet (108 CFU/g as HD). After 8-week feeding, growth performance, gut health index, serum enzyme activities and the expression of inflammation-related genes were tested. Results showed that the LD and HD diets had no adverse effects on the growth performance. Moreover, dietary HD enhanced gut barrier and reduced intestinal ROS and ORP, as well as increased serum enzyme activities including ACP, AKP, SOD and LZM compared to the CD group. In addition, the HD diet significantly up-regulated the expression of TNF-α, IL8, IL-1β and IL15, while down-regulating the expression of TGF-β1 and IL10 in kidney. Moreover, the expression of antibacterial genes was significantly increased in HD group after being challenged by N. seriolae. And the fish fed HD diet exhibited higher survival rate (57.5%) than that in CD (37.5%) and LD groups (42.5%). To summarize, our study demonstrates that dietary HD can enhance gut health, improve immune response and strengthen pathogen resistance, suggesting that C. somerae is a potential probiotic for defending against N. seriolae infection in M. salmoides.

The specific mitochondrial unfolded protein response in fast- and slow-twitch muscles of high-fat diet-induced insulin-resistant rats.

Skeletal muscle insulin resistance (IR) plays an important role in the pathogenesis of type 2 diabetes mellitus. Skeletal muscle is a heterogeneous tissue composed of different muscle fiber types that contribute distinctly to IR development. Glucose transport shows more protection in slow-twitch muscles than in fast-twitch muscles during IR development, while the mechanisms involved remain unclear. Therefore, we investigated the role of the mitochondrial unfolded protein response (UPRmt) in the distinct resistance of two types of muscle in IR. Male Wistar rats were divided into high-fat diet (HFD) feeding and control groups. We measured glucose transport, mitochondrial respiration, UPRmt and histone methylation modification of UPRmt-related proteins to examine the UPRmt in the slow fiber-enriched soleus (Sol) and fast fiber-enriched tibialis anterior (TA) under HFD conditions. Our results indicate that 18 weeks of HFD can cause systemic IR, while the disturbance of Glut4-dependent glucose transport only occurred in fast-twitch muscle. The expression levels of UPRmt markers, including ATF5, HSP60 and ClpP, and the UPRmt-related mitokine MOTS-c were significantly higher in slow-twitch muscle than in fast-twitch muscle under HFD conditions. Mitochondrial respiratory function is maintained only in slow-twitch muscle. Additionally, in the Sol, histone methylation at the ATF5 promoter region was significantly higher than that in the TA after HFD feeding. The expression of proteins involved in glucose transport in slow-twitch muscle remains almost unaltered after HFD intervention, whereas a significant decline of these proteins was observed in fast-twitch muscle. Specific activation of the UPRmt in slow-twitch muscle, accompanied by higher mitochondrial respiratory function and MOTS-c expression, may contribute to the higher resistance to HFD in slow-twitch muscle. Notably, the different histone modifications of UPRmt regulators may underlie the specific activation of the UPRmt in different muscle types. However, future work applying genetic or pharmacological approaches should further uncover the relationship between the UPRmt and insulin resistance.