-
Nutrients Jun 2024High-fat diets cause gut dysbiosis and promote triglyceride accumulation, obesity, gut permeability changes, inflammation, and insulin resistance. Both cocoa butter and...
BACKGROUND
High-fat diets cause gut dysbiosis and promote triglyceride accumulation, obesity, gut permeability changes, inflammation, and insulin resistance. Both cocoa butter and fish oil are considered to be a part of healthy diets. However, their differential effects on gut microbiome perturbations in mice fed high concentrations of these fats, in the absence of sucrose, remains to be elucidated. The aim of the study was to test whether the sucrose-free cocoa butter-based high-fat diet (C-HFD) feeding in mice leads to gut dysbiosis that associates with a pathologic phenotype marked by hepatic steatosis, low-grade inflammation, perturbed glucose homeostasis, and insulin resistance, compared with control mice fed the fish oil based high-fat diet (F-HFD).
RESULTS
C57BL/6 mice (5-6 mice/group) were fed two types of high fat diets (C-HFD and F-HFD) for 24 weeks. No significant difference was found in the liver weight or total body weight between the two groups. The 16S rRNA sequencing of gut bacterial samples displayed gut dysbiosis in C-HFD group, with differentially-altered microbial diversity or relative abundances. , and were highly abundant in C-HFD group, while the , (TM7), , and were more abundant in F-HFD group. Other taxa in C-HFD group included the (AF12), and An increased Firmicutes/Bacteroidetes (F/B) ratio in C-HFD group, compared with F-HFD group, indicated the gut dysbiosis. These gut bacterial changes in C-HFD group had predicted associations with fatty liver disease and with lipogenic, inflammatory, glucose metabolic, and insulin signaling pathways. Consistent with its microbiome shift, the C-HFD group showed hepatic inflammation and steatosis, high fasting blood glucose, insulin resistance, increased hepatic de novo lipogenesis (Acetyl CoA carboxylases 1 (), Fatty acid synthase (), Stearoyl-CoA desaturase-1 (), Elongation of long-chain fatty acids family member 6 (), Peroxisome proliferator-activated receptor-gamma () and cholesterol synthesis (β-(hydroxy β-methylglutaryl-CoA reductase (). Non-significant differences were observed regarding fatty acid uptake (Cluster of differentiation 36 (), Fatty acid binding protein-1 () and efflux (ATP-binding cassette G1 (), Microsomal TG transfer protein () in C-HFD group, compared with F-HFD group. The C-HFD group also displayed increased gene expression of inflammatory markers including Tumor necrosis factor alpha (), C-C motif chemokine ligand 2 (), and Interleukin-12 (), as well as a tendency for liver fibrosis.
CONCLUSION
These findings suggest that the sucrose-free C-HFD feeding in mice induces gut dysbiosis which associates with liver inflammation, steatosis, glucose intolerance and insulin resistance.
Topics: Animals; Dysbiosis; Gastrointestinal Microbiome; Insulin Resistance; Diet, High-Fat; Mice, Inbred C57BL; Male; Mice; Fatty Liver; Liver; Dietary Fats; Sucrose
PubMed: 38931284
DOI: 10.3390/nu16121929 -
Nutrients Jun 2024Gut microbiota are the microbial organisms that play a pivotal role in intestinal health and during disease conditions. Keeping in view the characteristic functions of...
Gut microbiota are the microbial organisms that play a pivotal role in intestinal health and during disease conditions. Keeping in view the characteristic functions of gut microbiota, in this study, TPC32 ( TPC32) was isolated and identified, and its whole genome was analyzed by the Illumina MiSeq sequencing platform. The results revealed that TPC32 had high resistance against acid and bile salts with fine in vitro antibacterial ability. Accordingly, a genome sequence of TPC32 has a total length of 2,214,495 base pairs with a guanine-cytosine content of 38.81%. Based on metabolic annotation, out of 2,212 protein-encoding genes, 118 and 101 were annotated to carbohydrate metabolism and metabolism of cofactors and vitamins, respectively. Similarly, drug-resistance and virulence genes were annotated using the comprehensive antibiotic research database (CARD) and the virulence factor database (VFDB), in which and drug-resistance genes were annotated in TPC32, while virulence genes are not annotated. The early prevention of TPC32 reduced the () infection in mice. The results show that TPC32 could improve the serum IgM, decrease the intestinal cytokine secretion to relieve intestinal cytokine storm, reinforce the intestinal biochemical barrier function by elevating the sIgA expression, and strengthen the intestinal physical barrier function. Simultaneously, based on the 16S rRNA analysis, the TPC32 results affect the recovery of intestinal microbiota from disease conditions and promote the multiplication of beneficial bacteria. These results provide new insights into the biological functions and therapeutic potential of TPC32 for treating intestinal inflammation.
Topics: Limosilactobacillus reuteri; Probiotics; Animals; Gastrointestinal Microbiome; Whole Genome Sequencing; Mice; Swine; Genome, Bacterial; Salmonella typhimurium; Anti-Bacterial Agents; Virulence Factors
PubMed: 38931255
DOI: 10.3390/nu16121900 -
Nutrients Jun 2024Advanced glycation end products (AGEs) accumulate in the plasma of pregnant women with hyperglycemia, potentially inducing oxidative stress and fetal developmental...
Advanced glycation end products (AGEs) accumulate in the plasma of pregnant women with hyperglycemia, potentially inducing oxidative stress and fetal developmental abnormalities. Although intrauterine hyperglycemia has been implicated in excessive fetal growth, the effects of maternal AGEs on fetal development remain unclear. We evaluated the differentiation regulators and cellular signaling in the skeletal muscles of infants born to control mothers (ICM), diabetic mothers (IDM), and diabetic mothers supplemented with either cis-palmitoleic acid (CPA) or trans-palmitoleic acid (TPA). Cell viability, reactive oxygen species levels, and myotube formation were assessed in AGE-exposed C2C12 cells to explore potential mitigation by CPA and TPA. Elevated receptors for AGE expression and decreased Akt and AMPK phosphorylation were evident in rat skeletal muscles in IDM. Maternal palmitoleic acid supplementation alleviated insulin resistance by downregulating RAGE expression and enhancing Akt phosphorylation. The exposure of the C2C12 cells to AGEs reduced cell viability and myotube formation and elevated reactive oxygen species levels, which were attenuated by CPA or TPA supplementation. This suggests that maternal hyperglycemia and plasma AGEs may contribute to skeletal muscle disorders in offspring, which are mitigated by palmitoleic acid supplementation. Hence, the maternal intake of palmitoleic acid during pregnancy may have implications for fetal health.
Topics: Fatty Acids, Monounsaturated; Glycation End Products, Advanced; Female; Animals; Pregnancy; Receptor for Advanced Glycation End Products; Rats; Muscle, Skeletal; Reactive Oxygen Species; Cell Line; Cell Survival; Mice; Dietary Supplements; Proto-Oncogene Proteins c-akt; Oxidative Stress; Insulin Resistance; Humans; Phosphorylation; Rats, Sprague-Dawley; Pregnancy in Diabetics; Male; Fetal Development
PubMed: 38931253
DOI: 10.3390/nu16121898 -
Nutrients Jun 2024Diabetes mellitus (DM) is a major risk and prognostic factor for heart failure (HF). Insulin resistance (IR) is an important component of DM, but the relationship...
Diabetes mellitus (DM) is a major risk and prognostic factor for heart failure (HF). Insulin resistance (IR) is an important component of DM, but the relationship between IR and HF prognosis has not yet been established across a wide variety of HF populations. We retrospectively evaluated the relationship between IR and clinical outcomes of HF patients at our hospital between 2017 and 2021. IR was defined as a homeostatic model assessment of IR (HOMA-IR) index ≥ 2.5, calculated from fasting blood glucose and insulin concentrations. The primary outcome was a composite of all-cause death and hospitalisation for HF (HHF). Among 682 patients included in the analyses, 337 (49.4%) had IR. The median age was 70 [interquartile range (IQR): 59-77] years old, and 66% of the patients were men. Among the patients, 41% had a left ventricular ejection fraction below 40%, and 32% had DM. The median follow-up period was 16.5 [IQR: 4.4-37.3] months. IR was independently associated with the primary outcome (HR: 1.91, 95% CI: 1.39-2.62, < 0.0001), death (hazard ratio [HR]: 1.86, 95% confidence interval [CI]: 1.28-2.83, < 0.01), and HHF (HR: 1.91, 95% CI: 1.28-2.83, < 0.01). HOMA-IR is an independent prognostic factor of HF in a wide variety of HF populations.
Topics: Humans; Insulin Resistance; Heart Failure; Male; Female; Aged; Middle Aged; Prognosis; Japan; Retrospective Studies; Blood Glucose; Hospitalization; Insulin; Risk Factors; Stroke Volume
PubMed: 38931242
DOI: 10.3390/nu16121888 -
Nutrients Jun 2024It is a common belief amongst strength and power athletes that nutritional supplementation strategies aid recovery by shifting the anabolic/catabolic profile toward... (Review)
Review
It is a common belief amongst strength and power athletes that nutritional supplementation strategies aid recovery by shifting the anabolic/catabolic profile toward anabolism. Factors such as nutrient quantity, nutrient quality, and nutrient timing significantly impact upon the effectiveness of nutritional strategies in optimizing the acute responses to resistance exercise and the adaptive response to resistance training (i.e., muscle growth and strength expression). Specifically, the aim of this review is to address carbohydrates (CHOs), protein (PRO), and/or amino acids (AAs) supplementation strategies, as there is growing evidence suggesting a link between nutrient signaling and the initiation of protein synthesis, muscle glycogen resynthesis, and the attenuation of myofibrillar protein degradation following resistance exercise. Collectively, the current scientific literature indicates that nutritional supplementation strategies utilizing CHO, PRO, and/or AA represents an important approach aimed at enhancing muscular responses for strength and power athletes, primarily increased muscular hypertrophy and enhanced strength expression. There appears to be a critical interaction between resistance exercise and nutrient-cell signaling associated with the principle of nutrient timing (i.e., pre-exercise, during, and post-exercise). Recommendations for nutritional supplementation strategies to promote muscular responses for strength and athletes are provided.
Topics: Humans; Dietary Supplements; Dietary Proteins; Dietary Carbohydrates; Resistance Training; Amino Acids; Athletes; Muscle, Skeletal; Muscle Strength; Sports Nutritional Physiological Phenomena
PubMed: 38931241
DOI: 10.3390/nu16121886 -
Nutrients Jun 2024Breast cancer is the most common tumor in women. Chemotherapy is the gold standard for cancer treatment; however, severe side effects and tumor resistance are the major... (Review)
Review
Breast cancer is the most common tumor in women. Chemotherapy is the gold standard for cancer treatment; however, severe side effects and tumor resistance are the major obstacles to chemotherapy success. Numerous dietary components and phytochemicals have been found to inhibit the molecular and signaling pathways associated with different stages of breast cancer development. In particular, this review is focused on the antitumor effects of PUFAs, dietary enzymes, and glucosinolates against breast cancer. The major databases were consulted to search in vitro and preclinical studies; only those with solid scientific evidence and reporting protective effects on breast cancer treatment were included. A consistent number of studies highlighted that dietary components and phytochemicals can have remarkable therapeutic effects as single agents or in combination with other anticancer agents, administered at different concentrations and via different routes of administration. These provide a natural strategy for chemoprevention, reduce the risk of breast cancer recurrence, impair cell proliferation and viability, and induce apoptosis. Some of these bioactive compounds of dietary origin, however, show poor solubility and low bioavailability; hence, encapsulation in nanoformulations are promising tools able to increase clinical efficiency.
Topics: Humans; Breast Neoplasms; Female; Phytochemicals; Diet; Chemoprevention; Drug Synergism; Animals; Antineoplastic Combined Chemotherapy Protocols; Glucosinolates
PubMed: 38931238
DOI: 10.3390/nu16121883 -
Nutrients Jun 2024Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease which seriously affects public health. Gut microbiota remains a dynamic balance state in healthy...
Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease which seriously affects public health. Gut microbiota remains a dynamic balance state in healthy individuals, and its disorder may affect health status and even results in metabolic diseases. Quercetin, a natural flavonoid, has been shown to have biological activities that can be used in the prevention and treatment of metabolic diseases. This study aimed to explore the mechanism of quercetin in alleviating T2DM based on gut microbiota. / mice were adopted as the model for T2DM in this study. After 10 weeks of administration, quercetin could significantly decrease the levels of body weight, fasting blood glucose (FBG), serum insulin (INS), the homeostasis model assessment of insulin resistance (HOMA-IR), monocyte chemoattractant protein-1 (MCP-1), D-lactic acid (D-LA), and lipopolysaccharide (LPS) in / mice. 16S rRNA gene sequencing and untargeted metabolomics analysis were performed to compare the differences of gut microbiota and metabolites among the groups. The results demonstrated that quercetin decreased the abundance of Proteobacteria, , and . Moreover, metabolomics analysis showed that the levels of L-Dopa and S-Adenosyl-L-methionine (SAM) were significantly increased, but 3-Methoxytyramine (3-MET), L-Aspartic acid, L-Glutamic acid, and Androstenedione were significantly decreased under quercetin intervention. Taken together, quercetin could exert its hypoglycemic effect, alleviate insulin resistance, repair the intestinal barrier, remodel the intestinal microbiota, and alter the metabolites of / mice.
Topics: Animals; Gastrointestinal Microbiome; Quercetin; Insulin Resistance; Mice; Diabetes Mellitus, Type 2; Male; Intestinal Mucosa; Blood Glucose; Disease Models, Animal; Insulin
PubMed: 38931226
DOI: 10.3390/nu16121870 -
Nutrients Jun 2024, a polyphenol-rich plant, holds potential for improving inflammation, but its mechanisms are not well understood. Therefore, this study employed network pharmacology...
, a polyphenol-rich plant, holds potential for improving inflammation, but its mechanisms are not well understood. Therefore, this study employed network pharmacology and molecular docking to explore the mechanism by which ameliorates inflammation. In this study, 29 kinds of active ingredients were obtained via data mining. Five main active components were screened out for improving inflammation, which were flemichin D, naringenin, chrysophanol, genistein and orobol. In total, 52 core targets were identified, including AKT serine/threonine kinase 1 (AKT1), tumor necrosis factor (TNF), B-cell lymphoma-2 (BCL2), serum albumin (ALB), and estrogen receptor 1 (ESR1). Gene ontology (GO) enrichment analysis identified 2331 entries related to biological processes, 98 entries associated with cellular components, and 203 entries linked to molecular functions. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis yielded 149 pathways, including those involved in EGFR tyrosine kinase inhibitor resistance, endocrine resistance, and the PI3K-Akt signaling pathway. Molecular docking results showed strong binding effects between the main active components and the core targets, with binding energies less than -5 kcal/mol. In summary, this study preliminarily elucidated the underlying mechanisms by which , through a multi-component, multi-target, and multi-pathway approach, ameliorates inflammation. This provides a theoretical foundation for the subsequent application of in inflammation amelioration.
Topics: Molecular Docking Simulation; Network Pharmacology; Inflammation; Humans; Signal Transduction; Fabaceae; Anti-Inflammatory Agents; Proto-Oncogene Proteins c-akt; Plant Extracts
PubMed: 38931205
DOI: 10.3390/nu16121850 -
Nutrients Jun 2024In order to better understand which metabolic differences are related to insulin resistance in metabolic syndrome (MetSyn), we used hyperinsulinemic-euglycemic (HE)...
CONTEXT/OBJECTIVE
In order to better understand which metabolic differences are related to insulin resistance in metabolic syndrome (MetSyn), we used hyperinsulinemic-euglycemic (HE) clamps in individuals with MetSyn and related peripheral insulin resistance to circulating biomarkers.
DESIGN/METHODS
In this cross-sectional study, HE-clamps were performed in treatment-naive men (n = 97) with MetSyn. Subjects were defined as insulin-resistant based on the rate of disappearance (Rd). Machine learning models and conventional statistics were used to identify biomarkers of insulin resistance. Findings were replicated in a cohort with n = 282 obese men and women with (n = 156) and without (n = 126) MetSyn. In addition to this, the relation between biomarkers and adipose tissue was assessed by nuclear magnetic resonance imaging.
RESULTS
Peripheral insulin resistance is marked by changes in proteins related to inflammatory processes such as IL-1 and TNF-receptor and superfamily members. These proteins can distinguish between insulin-resistant and insulin-sensitive individuals (AUC = 0.72 ± 0.10) with MetSyn. These proteins were also associated with IFG, liver fat (rho 0.36, = 1.79 × 10) and visceral adipose tissue (rho = 0.35, = 6.80 × 10). Interestingly, these proteins had the strongest association in the MetSyn subgroup compared to individuals without MetSyn.
CONCLUSIONS
MetSyn associated with insulin resistance is characterized by protein changes related to body fat content, insulin signaling and pro-inflammatory processes. These findings provide novel targets for intervention studies and should be the focus of future in vitro and in vivo studies.
Topics: Humans; Insulin Resistance; Metabolic Syndrome; Male; Female; Cross-Sectional Studies; Middle Aged; Adult; Biomarkers; Proteome; Glucose Clamp Technique; Obesity; Adipose Tissue; Insulin; Intra-Abdominal Fat
PubMed: 38931177
DOI: 10.3390/nu16121822 -
Nutrients Jun 2024The global rise in type 2 diabetes (T2D) and obesity necessitates innovative dietary interventions. This study investigates the effects of allulose, a rare sugar shown...
The global rise in type 2 diabetes (T2D) and obesity necessitates innovative dietary interventions. This study investigates the effects of allulose, a rare sugar shown to reduce blood glucose, in a rat model of diet-induced obesity and T2D. Over 12 weeks, we hypothesized that allulose supplementation would improve body weight, insulin sensitivity, and glycemic control. Our results showed that allulose mitigated the adverse effects of high-fat, high-sugar diets, including reduced body weight gain and improved insulin resistance. The allulose group exhibited lower food consumption and increased levels of glucagon-like peptide-1 (GLP-1), enhancing glucose regulation and appetite control. Additionally, allulose prevented liver triglyceride accumulation and promoted mitochondrial uncoupling in adipose tissue. These findings suggest that allulose supplementation can improve metabolic health markers, making it a promising dietary component for managing obesity and T2D. Further research is needed to explore the long-term benefits and mechanisms of allulose in metabolic disease prevention and management. This study supports the potential of allulose as a safe and effective intervention for improving metabolic health in the context of dietary excess.
Topics: Animals; Fructose; Male; Obesity; Diabetes Mellitus, Type 2; Insulin Resistance; Blood Glucose; Rats; Diet, High-Fat; Liver; Glucagon-Like Peptide 1; Triglycerides; Rats, Sprague-Dawley; Adipose Tissue; Weight Gain; Disease Models, Animal
PubMed: 38931176
DOI: 10.3390/nu16121821