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Nutrition & Diabetes Jun 2024Clinical guidelines recommend basic carbohydrate counting (BCC), or similar methods to improve carbohydrate estimation skills and to strive for higher consistency in... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND
Clinical guidelines recommend basic carbohydrate counting (BCC), or similar methods to improve carbohydrate estimation skills and to strive for higher consistency in carbohydrate intake potentially improving glycaemic control. However, evidence for this approach in type 2 diabetes (T2D) is limited.
OBJECTIVE
To examine the efficacy of a structured education program in BCC as add-on to standard dietary care on glycaemic control in individuals with T2D.
METHODS
The BCC Study was a randomized, controlled, open-label, parallel-group trial. Individuals with T2D aged 18-75 years with glycated haemoglobin A1c (HbA1c) 53-97 mmol/mol (7.0-11.0%) were randomly assigned (1:1) to BCC or standard dietary care. The primary outcomes were differences in changes in HbA1c or glycaemic variability (calculated as mean amplitude of glycaemic excursions [MAGE]) between groups after six months of intervention.
RESULTS
Between September 2018 and July 2021, 48 participants were randomly assigned, 23 to BCC and 25 to standard dietary care. Seven participants did not receive the allocated intervention. From a baseline-adjusted mean of 65 mmol/mol (95% CI 62-68 [8.1%, 7.8-8.4]), HbA1c changed by -5 mmol/mol (-8 to -1 [-0.5%, -0.7 to -0.1]) in BCC and -3 mmol/mol (-7 to 1 [-0.3%, -0.6 to 0.1]) in standard care with an estimated treatment effect of -2 mmol/mol (-7 to 4 [-0.2%, -0.6 to 0.4]); p = 0.554. From a baseline-adjusted mean of 4.2 mmol/l (3.7 to 4.8), MAGE changed by -16% (-33 to 5) in BCC and by -3% (-21 to 20) in standard care with an estimated treatment effect of -14% (-36 to 16); p = 0.319. Only median carbohydrate estimation error in favour of BCC (estimated treatment difference -55% (-70 to -32); p < 0.001) remained significant after multiple testing adjustment.
CONCLUSIONS
No glycaemic effects were found but incorporating BCC as a supplementary component to standard dietary care led to improved skills in estimating carbohydrate intake among individuals with T2D.
Topics: Humans; Diabetes Mellitus, Type 2; Middle Aged; Male; Female; Glycemic Control; Glycated Hemoglobin; Aged; Blood Glucose; Adult; Dietary Carbohydrates; Patient Education as Topic; Adolescent; Young Adult; Diet, Carbohydrate-Restricted; Treatment Outcome
PubMed: 38937460
DOI: 10.1038/s41387-024-00307-0 -
In Vivo (Athens, Greece) 2024This study examined the effects of tocotrienols (TT) in conjunction with statin on glucose homeostasis, bone microstructure, gut microbiome, and systemic and liver...
BACKGROUND/AIM
This study examined the effects of tocotrienols (TT) in conjunction with statin on glucose homeostasis, bone microstructure, gut microbiome, and systemic and liver inflammatory markers in obese C57BL/6J mice.
MATERIALS AND METHODS
Forty male C57BL/6J mice were fed a high-fat diet (HFD) and assigned into four groups in a 2 (no statin vs. 120 mg statin/kg diet)×2 (no TT vs. 400 mg TT/kg diet) factorial design for 14 weeks.
RESULTS
Statin and TT improved glucose tolerance only when each was given alone, and only statin supplementation decreased insulin resistance. Consistently, only statin supplementation decreased serum insulin levels and HOMA-IR. Pancreatic insulin was also increased with statin treatment. Statin and TT, alone or in combination, reduced the levels of serum IL-6, but only TT attenuated the increased serum leptin levels induced by a HFD. Statin supplementation increased bone area/total area and connectivity density at LV-4, while TT supplementation increased bone area/total area and trabecular number, but decreased trabecular separation at the distal femur. Statin supplementation, but not TT, reduced hepatic inflammatory cytokine gene expression. Neither TT supplementation nor statin supplementation statistically altered microbiome species evenness or richness. However, they altered the relative abundance of certain microbiome species. Most notably, both TT and statin supplementation increased the relative abundance of Lachnospiraceae UCG-006.
CONCLUSION
TT and statin collectively benefit bone microstructure, glucose homeostasis, and microbial ecology in obese mice. Such changes may be, in part, associated with suppression of inflammation in the host.
Topics: Animals; Gastrointestinal Microbiome; Tocotrienols; Mice; Homeostasis; Obesity; Male; Dietary Supplements; Bone and Bones; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Diet, High-Fat; Bixaceae; Mice, Obese; Plant Extracts; Glucose; Mice, Inbred C57BL; Insulin Resistance; Blood Glucose; Disease Models, Animal; Liver; Biomarkers; Carotenoids
PubMed: 38936927
DOI: 10.21873/invivo.13606 -
Journal of the Academy of Nutrition and... Jun 2024
PubMed: 38936770
DOI: 10.1016/j.jand.2024.06.222 -
Molecular Metabolism Jun 2024The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) continues to rise with the increasing obesity epidemic. Rezdiffra as an activator of a...
OBJECTIVE
The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) continues to rise with the increasing obesity epidemic. Rezdiffra as an activator of a thyroid hormone receptor-beta is the only Food and Drug Administration approved therapy. As such, there is a critical need to improve our understanding of gene expression regulation and signaling transduction in MASLD to develop new therapies. Matrin-3 is a DNA- and RNA-binding protein involved in the pathogenesis of human diseases. Here we examined its previously uncharacterized role in limiting hepatic steatosis and stress response via the constitutive androstane receptor (CAR).
METHODS
Matrin-3 floxed and liver-specific knockout mice were fed either a chow diet or 60 kcal% high-fat diet (HFD) for up to 16 weeks. The mice were euthanized for different analysis including liver histology, lipid levels, and gene expression. Bulk RNA-seq, bulk ATAC-seq, and single-nucleus Multiome were used to examine changes of transcriptome and chromatin accessibility in the liver. Integrative bioinformatics analysis of our data and publicly available datasets and different biochemical assays were performed to identify underlying the molecular mechanisms mediating matrin-3's effects. Liver-tropic adeno-associated virus was used to restore the expression of CAR for lipid, acute phase genes, and histological analysis.
RESULTS
Matrin-3 expression is induced in the steatotic livers of mice. Liver-specific matrin-3 deletion exacerbated HFD-induced steatosis, acute phase response, and inflammation in the liver of female mice. The transcriptome and chromatin accessibility were re-programmed in the liver of these mice with signatures indicating that CAR signaling is dysregulated. Mechanistically, matrin-3 interacts with CAR mRNA, and matrin-3 deficiency promotes CAR mRNA degradation. Consequently, matrin-3 deletion impaired CAR signaling by reducing CAR expression. Matrin-3 levels positively correlate with CAR expression in human livers. Ces2a and Il1r1 were identified as new target genes of CAR. Interestingly, we found that CAR discords with the expression of its target genes including Cyp2b10 and Ces2a in response to HFD, indicating CAR signaling is dysregulated by HFD despite increased CAR expression. Dysregulated CAR signaling upon matrin-3 deficiency reduced Ces2a and de-repressed Il1r1 expression. CAR restoration partially abrogated the dysregulated gene expression, exacerbated hepatic steatosis, acute phase response, and inflammation in liver-specific matrin-3 knockout mice fed a HFD.
CONCLUSIONS
Our findings demonstrate that matrin-3 is a key upstream regulator maintaining CAR signaling upon metabolic stress, and the matrin-3-CAR axis limits hepatic steatosis and stress response signaling that may give insights for therapeutic intervention.
PubMed: 38936659
DOI: 10.1016/j.molmet.2024.101977 -
The Journal of Nutrition Jun 2024Infertility impacts 16% of North American couples, with male factor infertility contributing to ∼30% of cases. Reproductive hormones, especially testosterone, are...
BACKGROUND
Infertility impacts 16% of North American couples, with male factor infertility contributing to ∼30% of cases. Reproductive hormones, especially testosterone, are essential for spermatogenesis. Age-independent population-level decline in testosterone concentrations over the past few decades has been proposed to be a result of diet and lifestyle changes. Vitamin B is present in the testes and has been suggested as an adjuvant nutritional therapy for male infertility due to its potential to improve sperm parameters. However, evidence examining the relationship between vitamin B and reproductive hormones is limited.
OBJECTIVE
The objective was to cross-sectionally examine the relationship between serum vitamin B and male reproductive hormones (luteinizing hormone, follicular stimulating hormone, total testosterone, estradiol and prolactin).
METHODS
Men with infertility (n = 303) were recruited from Mount Sinai Hospital in Toronto, Canada. Serum was analyzed for vitamin B and reproductive hormones. Statistical analyses included non-parametric Spearman's rank correlation coefficient, linear regression, logistic regression and effect modification by age and BMI linear regressions.
RESULTS
An independent monotonic relationship between serum vitamin B and total testosterone (rho = 0.19, P = 0.001) was observed. Serum vitamin B was linearly associated with total testosterone (unadjusted ß = 0.0007, P = 0.008 and adjusted ß = 0.0005, P = 0.03). Compared to individuals in the lowest tertile of serum vitamin B, those in the middle tertile (adjusted OR = 0.48, 95% CI [0.25, 0.93], P = 0.03) and the highest tertile (unadjusted OR = 0.41, 95% CI [0.22, 0.77], P = 0.005 and adjusted OR = 0.44, 95% CI [0.22, 0.87], P = 0.02) had reduced odds of testosterone deficiency.
CONCLUSIONS
These findings suggest that among men with infertility, low serum vitamin B is associated with higher risk of testosterone deficiency and impaired androgenic hormonal profiles that impact spermatogenesis and consequently, fertility.
PubMed: 38936552
DOI: 10.1016/j.tjnut.2024.06.013 -
Current Opinion in Gastroenterology Jun 2024The purpose of this review was to highlight most recent updates on nutritional aspects in gastroparesis (GP) focusing on dietary recommendations, utilization of enteral...
PURPOSE OF THE REVIEW
The purpose of this review was to highlight most recent updates on nutritional aspects in gastroparesis (GP) focusing on dietary recommendations, utilization of enteral and parenteral nutrition, endoscopic and surgical interventions.
RECENT FINDINGS
Recent data addressed eating patterns, nutritional interventions, and clarifications on the role of endoscopic and surgical interventions underlying an impact on nutritional management of GP patients. They support the importance of gastroparesis-specific diet in addition to drug therapy, and confirm the benefits of a modified low-fat, low-fiber diet. Current guidelines suggest a new approach to GP management based on predominant symptoms. Gastric peroral endoscopic pyloromyotomy (G-POEM) and surgical gastric electrical stimulator (GES) placement may be considered in individuals with nausea and vomiting before the need for jejunostomy tube placement for enteral feeding or parenteral nutrition.
SUMMARY
Current literature supports the importance of dietary interventions, focusing on low-fat and low-fiber diets, in addition to drug therapies. Severely fiber-restrictive diets may not be necessary. There is enhanced understanding when jejunal feeding should be incorporated for refractory cases with consideration of G-POEM or/and GES even before jejunal tube placement. This approach will require patient evaluation in specialized motility centers.
PubMed: 38935298
DOI: 10.1097/MOG.0000000000001050 -
Zeitschrift Fur Rheumatologie Jun 2024Patients with diseases of the musculoskeletal system are confronted with a large quantity of treatment offers based on methods of complementary medicine. Despite...
Patients with diseases of the musculoskeletal system are confronted with a large quantity of treatment offers based on methods of complementary medicine. Despite a considerable number of publications on this topic, the scientific evidence is still poor. This article focuses on Ayurvedic medicine (AM), traditional Chinese medicine (TCM), mind-body medicine and homeopathy. These procedures have a longstanding tradition of practice and each claims to have its own theoretical concept; however, the application in the field of rheumatology can only be recommended either for specific entities or, in the case of homeopathy, not at all. In addition, this article summarizes the evidence for dietary recommendations, nutritional supplements and herbal medicine in rheumatology. The latter topics are frequently discussed in the popular press and are a much-debated issue between physicians and patients; however, clear-cut recommendations for the application on a scientific basis are the exception and mainly consist of the endorsement to adhere to the principles of a Mediterranean diet.
PubMed: 38935116
DOI: 10.1007/s00393-024-01524-9 -
International Journal of Surgery... Jun 2024Bone and joint infections (BJI) are a significant complication after arthroplasty and fracture fixation, particularly challenging in patients with type 2 diabetes...
BACKGROUND
Bone and joint infections (BJI) are a significant complication after arthroplasty and fracture fixation, particularly challenging in patients with type 2 diabetes mellitus (T2DM) and obesity. Semaglutide, a glucagon-like peptide-1 receptor agonist (GLP-1RA), have shown efficacy in managing T2DM and obesity. However, its impact on BJI risk and neutrophil function remains unclear. To investigate whether preoperative semaglutide treatment (1) reduces the risk of BJI in diabetic and obese mice undergoing intra-articular implants, and (2) outperforms insulin in restoring neutrophil function to mitigate implant-related infection.
METHODS
A C57BL/6 mouse model of T2DM/obesity was induced using a high-fat diet (HFD) for 12 weeks. Mice received preoperative insulin or semaglutide therapy for 1-28 days. BJI risk was assessed using an intraarticular-implant model challenged with S. aureus or E. coli. Neutrophil function was evaluated through bactericidal activity, superoxide production, and migration ability.
RESULTS
Semaglutide treatment led to a significant and sustained reduction in body weight and improved glucose tolerance in HFD mice. Both insulin and semaglutide therapies significantly reduced BJI risk, with semaglutide showing a more pronounced effect over time. Semaglutide therapy also enhanced neutrophil bactericidal activity, superoxide production, and migration ability compared to insulin therapy.
CONCLUSIONS
Preoperative semaglutide treatment effectively reduces BJI risk and improves neutrophil function in diabetic and obese mouse models. These findings suggest that semaglutide may be a promising pharmacological intervention to mitigate infection risk in orthopedic patients with T2DM or obesity.
PubMed: 38935106
DOI: 10.1097/JS9.0000000000001896 -
Endocrinology Jun 2024Thyroid hormone (TH) plays a crucial role in regulating the functions of both bone and adipose tissue. Given that TH exerts its cholesterol-lowering effects in hepatic...
Thyroid hormone (TH) plays a crucial role in regulating the functions of both bone and adipose tissue. Given that TH exerts its cholesterol-lowering effects in hepatic tissue through the TH receptor-β (TRβ), we hypothesized that TRβ agonist therapy using MGL3196 (MGL) would be effective in treating increased adiposity and bone loss in response to a 12-week high-fat diet (HFD) in adult C57BL/6J mice. Transcriptional and serum profiling revealed that HFD-induced Leptin promoted weight gain in both males and females, but MGL only suppressed Leptin induction and weight gain in males. In vitro studies suggest estrogen suppresses MGL activity in adipocytes, indicating estrogen might interfere with MGL-TRβ function. Compared to systemic adiposity, HFD reduced bone mass in male but not female mice. Paradoxically, MGL treatment reversed macroscopic BMD loss in appendicular bones, but micro-CT revealed that MGL exacerbated HFD-induced trabecular bone loss, and bone strength. In studies on the mechanisms for HFD effects on bone, we found that HFD induced Rankl expression in male femurs that was blocked by MGL. By ex vivo assays, we found that RANKL indirectly represses osteoblast lineage allocation of osteoprogenitors by induction of inflammatory cytokines TNFα, Il-1β, and CCL2. Finally, we found that MGL functions in both systemic adiposity and bone by nongenomic TRβ signaling, as HFD-mediated phenotypes were not rescued in TRβ147F knockout mice with normal genomic but defective nongenomic TRβ signaling. Our findings demonstrate that the negative effects of HFD on body fat and bone phenotypes is impacted by MGL in a gender-specific manner.
PubMed: 38935021
DOI: 10.1210/endocr/bqae075 -
Edible bird's nest regulates glucose and lipid metabolic disorders the gut-liver axis in obese mice.Food & Function Jun 2024Edible bird's nest (EBN) is a traditional food known for its nourishing and functional properties and is found to be involved in anti-oxidation, anti-aging, and...
Edible bird's nest (EBN) is a traditional food known for its nourishing and functional properties and is found to be involved in anti-oxidation, anti-aging, and anti-influenza mechanisms, immune regulation, and improving cardiovascular diseases, among others. However, the potential of EBN to improve glycolipid metabolism disorders in high-fat-diet induced obesity and the underlying mechanisms remain unexplored. We examined the effects of EBN on glycolipid metabolism in obese mice fed a high-fat diet. Male C57BL/6J mice were fed a high-fat diet for 8 weeks to establish an obesity model. The obese mice were selected and divided into six groups: two model control groups (normal and high-fat diets) and four intervention groups [Neu5Ac and low-, medium-, and high-dose EBN], with 12 mice in each group. After 10 weeks of continuous gavage intervention, only mice in the high-dose EBN intervention group had lower body weight and total fat content, especially visceral fat. Meanwhile, intervention with three doses of EBN reduced serum FBG, TC, LDL, Ox-LDL, IL-1β, IL-6, and TNF-α levels and increased serum HDL levels and energy expenditure. Using the high dosage as a paradigm, EBN intervention increased the sialic acid content in LDL, decreased TMAO in the liver, and increased GLP-1 levels in sera. EBN increased the colonic abundances of , , and and reduced those of and . The changes in the microbial community contribute to increasing colonic bile acids, reducing lipopolysaccharide synthesis to protect the intestinal barrier, and lowering inflammation levels. Changes were also observed in colonic transcripts and metabolites and liver gene transcripts and metabolites, which were mainly enriched in pathways of glycolipid metabolism, immune function amelioration, inflammatory signal mitigation, circadian rhythm, bile acid metabolism and insulin resistance. Therefore, EBN may enhance the gut microbiota and intestinal immunity, relieve chronic inflammation levels in serum, improve antioxidant capacity and circadian rhythm in the liver, promote bile acid metabolism, and decrease lipid absorption and lipid synthesis the gut-liver axis. Consequently, this may reduce blood lipid and fat accumulation as well as improve islet function and reduce blood glucose levels.
PubMed: 38934780
DOI: 10.1039/d4fo00563e