Nutrition & Diabetes最新文献

Background: Prediabetes is becoming increasingly widespread and often progresses to diabetes, thereby raising the risk of severe complications. High-protein diets, known to improve glucose control and prevent diabetes, can utilize rich-protein oral nutritional supplements. The study aims to evaluate the effectiveness of a diabetes-specific nutritional formula-pro (DSNF-Pro) with high-protein content and evaluate its clinical utility.

Methods: An open-label, cross-over clinical trial was conducted to compare the effects of DSNF-Pro versus Standard nutritional formula (STNF) on postprandial glycemic control. Fifteen subjects with prediabetes were enrolled and consumed DSNF-Pro on the first visit and STNF on the second. Postprandial plasma glucose, serum insulin, and serum c-peptide incremental area under the curve (iAUC), as well as the maximum concentration (C_max) and incremental maximal concentration (iC_max), were measured following the study. Statistical comparisons between DSNF-Pro and STNF were performed using Wilcoxon's signed-rank test.

Results: DSNF-Pro significantly reduced postprandial glucose iAUC by 73.4% (p = 0.0001) and postprandial c-peptide iAUC by 36.4% (p = 0.0001) compared to STNF. However, there was no significant difference in postprandial insulin iAUC between DSNF-Pro and STNF.

Conclusions: These results demonstrated that DSNF-Pro effectively improved postprandial glucose responses in prediabetes, providing a practical alternative for managing glycemic control without increasing insulin secretion.

Background/objectives: Diabetic nephropathy (DN) is a prevalent microvascular diabetic complication that is not totally unveiled. In this study, we considered GAS6, AXL, GAS6-AS1, and GAS6-DT as possible early diagnostic biomarkers of DN.

Subjects/methods: The study included 70 patients with normoalbuminuria type 2 diabetes (DM), 70 patients with microalbuminuria type 2 diabetes (DN), and 60 apparently healthy controls. Fasting plasma glucose, glycosylated hemoglobin, and plasma creatinine were enzymatically assayed. Albuminuria, plasma GAS6, and AXL levels were determined using ELISA. Long non-coding RNAs GAS6-AS1 and GAS6-DT levels were determined in blood using qRT-PCR. Several bioinformatics databases were employed to suggest interactions with the studied biomolecules.

Results: GAS6 and AXL were downregulated in DM + DN compared to controls, being the lowest in DN (p < 0.0001). GAS6-DT was upregulated in DM + DN compared to controls, being the highest in DN (p < 0.0001). GAS6-AS1 was higher in DN than in controls (p = 0.013). GAS6, AXL, and GAS6-DT showed fair-to-moderate significant correlations with HbA1c, fasting glucose, creatinine, and albuminuria. ROC curves showed remarkable diagnostic power of GAS6, AXL, and GAS6-DT (AUC = 0.72-1.0), but not GAS6-AS1, in DN and DM, with moderate-to-excellent agreement with conventional diagnostics.

Conclusions: The current findings emphasize the significance of the GAS6/AXL pathway in DM and DN progression, where GAS6, AXL, and GAS6-DT showed significantly altered values in DM, and further in DN, with notable diagnostic power for both diseases. To date, this is the first study confirming the diagnostic power of AXL and GAS6-DT in DN and DM. Future studies are warranted to evaluate therapeutically targeting this pathway to manage DN.

Background: Few studies evaluated the effect of different proportions of dietary plant- and animal-based protein on metabolic syndrome (MetS) and its related biomarkers.

Objective: Considering the effect of various types of dietary sources of protein on metabolic health and inconsistent results, this study sought to examine the impact of partially substituting animal protein with plant protein in the diet on the components of MetS, atherogenic index of plasma, and serum adropin values.

Methods: In this parallel, randomized clinical trial with two arms, 73 participants with MetS were randomly allocated to one of two slightly calorie-restricted intervention diets with different proportions of protein sources, including a plant-based protein diet (70% plant-based protein and 30% animal-based protein) and an animal-based protein diet (30% plant-based protein and 70% animal-based protein) for 10 weeks. All analyses were performed based on both intention-to-treat and per-protocol principles.

Results: Mean age in the plant and animal-based protein groups was 44.0 ± 9.8 and 43.9 ± 9.8 years, respectively. Within each group, weight, body mass index, systolic and diastolic blood pressure, and atherogenic index of plasma significantly decreased, and adropin levels significantly increased after the intervention (P < 0.05). However, waist circumference (WC) and triglyceride (TG) levels showed a significant decrease only in the plant protein group, and high-density lipoprotein cholesterol (HDL-c) levels illustrated a significant increase only in the animal protein group (P < 0.05). Between-group differences in both crude and adjusted models did not show any significant changes between the two intervention arms (P > 0.05). However, findings of per-protocol analyses illustrated a significant difference only in mean adropin values in two study arms.

Conclusion: Our findings revealed that both diets based on plant and animal protein were associated with improved in anthropometric indices, MetS components, atherogenic index of plasma, and elevated serum adropin levels. Nevertheless, no statistically significant difference was identified between the two groups.

Background: SGLT2 inhibitors (SGLTi) confer significant cardiometabolic benefits in diabetes, but are associated with increased risk of diabetic ketoacidosis (DKA). We hypothesized that supporting anaplerosis with glycerol could mitigate SGLTi-induced ketosis, enhance insulin-mediated resolution of severe diabetic ketosis, and lower the risk of DKA when used as a dietary supplement.

Methods: Insulin-dependent diabetes was induced in yearling sheep using alloxan. The animals subsequently developed severe hyperglycemia (glucose > 500 mg/dL) and hyperketonemia (β-hydroxybutyrate [BHB] > 5 mM), requiring daily insulin therapy for metabolic control and survival. Ketosis was induced by partial insulin withdrawal and with the administration of 10 mg of the SGLT2 inhibitor empagliflozin. Animals were randomly assigned in a cross-over trial to evaluate the effects of intravenous 5% glycerol infusions for the treatment of moderate diabetic ketosis (1.5 mM < BHB < 3.0 mM), and as an insulin-adjunct therapy in cases of severe diabetic ketosis (BHB > 3.0 mM). Longer-term effects of dietary glycerol were assessed by supplementing 5% glycerol in the drinking water of the diabetic sheep under empagliflozin treatment. Data were analyzed using repeated measures ANOVA with a standard least squares fit model in JMP.

Results: Intravenous glycerol administration decreased moderate ketosis by 28.5% (P = 0.03), increased glucose by 63.3% (P = 0.04), and enhanced insulin-mediated resolution of severe diabetic ketosis (P = 0.001). Nightly dietary glycerol intake suppressed empagliflozin-induced morning elevations in blood BHB (P = 0.002).

Conclusions: Intravenous glycerol reduced empagliflozin-induced ketosis and provided protection against hypoglycemia. When used as an insulin adjunct, it enhanced insulin resolution of severe diabetic ketosis induced by empagliflozin. Dietary glycerol supplementation improved the energetic state and reduced the risk of ketosis in diabetic sheep undergoing SGLTi therapy. These findings may have clinical relevance for DKA management and nutritional prevention, particularly but not necessarily under SGLTi therapy.

Background: Prediabetes is a public health concern, and its prevalence is growing around the world. Providing an effective strategy to prevent prediabetes progression and, consequently, type-2 diabetes mellitus (T2DM) could be useful for global health. The present study aimed to investigate the impact of vitamin D supplementation on metabolic factors, serum omentin-1 levels, and anthropometric indices in women with prediabetes.

Methods: This randomized controlled trial (RCT) study was carried out on women with prediabetes aged 18-65 years. The women were allocated to the intervention (n = 48) or placebo (n = 48) groups to receive vitamin D (50000 IU) or a placebo every two weeks for 12 weeks, respectively. Fasting blood samples, anthropometric measurements, and information about the dietary intake and physical activity of the participants were collected at the beginning and after the intervention. Data analyses were done using IBM SPSS Statistics software.

Results: Vitamin D intervention significantly enhanced 25-hydroxyvitamin D (MD (CI 95%): 11.610 ng/ml (8.264, 14.956)), insulin (MD (CI 95%): 0.413 µIU/mL (0.321, 0.505)), Homeostatic Model Assessment of Insulin Resistance (MD (CI 95%): 0.411 (0.319, 0.502)), and Homeostatic Model Assessment of Insulin Resistance-β cell function (MD (CI 95%): 29.505% (22.114, 36.986)) levels compared to the placebo at the end of trial (all, p < 0.05). Moreover, a significant reduction in QUICKI was observed after the intervention (MD (CI 95%): -0.062 (-0.076, -0.048)). Changes in fasting blood sugar (FBS), lipid profiles, omentin-1 levels, and anthropometric indices were not significant between the groups after the intervention.

Conclusion: The findings revealed that vitamin D administration improved insulin secretion but failed to affect FBS, lipid profiles, anthropometric indices, and body composition in women with prediabetes. Due to inconsistent results, more well-designed RCTs are required to clarify the effects of vitamin D supplementation on these patients.

Background: Temporal distribution and amplitude of physical activity/inactivity in 24 h known as circadian rest-activity rhythm may predict the risk of various metabolic diseases, including type 2 diabetes (T2D), yet the mechanisms behind the diurnal behavior patterns remain largely unexplored.

Methods: This study included 74,165 UK Biobank participants who were free of T2D at baseline. Circadian rest-activity rhythm (CRAR) characteristics, including amplitude (strength), acrophase (timing of peak activity), pseudo-F (robustness), and mesor (height), were assessed using an extended cosine model applied to accelerometer data. T2D was assessed using the established UK Biobank algorithms. Using Cox regression and restricted cubic spline models, we examined the association between CRAR and incident T2D as well as subsequent all-cause mortality among individuals developed T2D during the follow-up. Mediation analysis explored the mediating effects of blood and metabolic biomarkers.

Results: During a median follow-up of 7.9 years, 1784 T2D cases were documented. We found that CRAR abnormalities was associated with a higher risk of incident T2D compared to optimal CRAR, and the multivariate adjusted hazard ratios (HRs) (95% CI) were 1.48 (1.31, 1.67) for low amplitude, 1.25 (1.07, 1.45) for delayed acrophase, 1.17 (1.04, 1.31) for pseudo-F, and 1.55 (1.38, 1.74) for low mesor. Furthermore, low amplitude and low mesor were associated with higher all-cause mortality following the diagnosis of T2D. Serum vitamin D emerged as a crucial mediator in the association between CRAR abnormalities and the risk of T2D as well as subsequent all-cause mortality.

Conclusion: Our study suggests that CRAR abnormalities are linked to an elevated risk of incident T2D and subsequent mortality. These associations are mediated by blood and metabolic biomarkers, with serum vitamin D playing a significant role as the primary mediator.

Background: Prediabetes (PD) precedes type 2 diabetes (T2D), it can be easily recognized by fasting plasma glucose concentrations (FPG) or HbA1c or 2 h post glucose load glycemia, thereby enabling prevention strategies. We investigated the progression of PD to T2D in the ABCD study (Alimentazione, Benessere Cardiovascolare e Diabete -ISRCTN15840340) that included a representative cohort of adult people living in the Mediterranean area of Palermo (Italy).

Materials and methods: The ABCD cohort was enrolled in 2011 and re-evaluated in 2015. The FPG, HbA1c, physical activity level and dietary habits were investigated. In 2011 participants and their family doctors were informed about their health conditions and indications concerning realistic changes for a healthier lifestyle were provided.

Results: Complete information was obtained on 742 out of 1233 individuals. In 2011, the prevalence of PD was 30.7% of which 12.7% developed T2D and 43.9% reversed to normal glucose tolerance (NGT) at follow-up. In 2015, 106 previously NGT participants developed PD. The progression as to T2D as to PD were associated with age (P < 0.001) and sex (P < 0.001). Body weight, BMI, and waist circumference were higher in people with PD than in those without PD and even higher in PD that developed T2D (P < 0.001). A sedentary lifestyle was observed in the PD and NGT subgroups which developed T2D and PD, respectively. Daily energy intake decreased among people with PD who became NGT (P < 0.001) and increased in those who developed T2D (P < 0.05). The glycemic index of diet decreased in those PD people who became NGT and in those people who maintained NGT at follow-up. The MEDILITE score, that describes the Mediterranean pattern of diet, increased significantly in PD group that became NGT and in NGT group that maintained NGT at final observation.

Conclusions: This study suggests that improving individual motivation may be an effective strategy to promote healthier lifestyles. A more physically active lifestyle and Mediterranean dietary habits are associated with a reduction of central obesity, and with a favorable evolution of glucose tolerance in PD people.

Clinical trial registration: ISRCTN15840340.

Background & aims: Ketogenic diet (KD) is recognized as an effective lifestyle intervention for managing metabolic dysfunction-associated steatotic liver disease (MASLD). This research aimed to assess the impact of KD on metabolic parameters in MASLD mice and elucidate the underlying mechanism.

Methods: High-fat diet (HFD)-induced MASLD mice were subjected to KD for 2 weeks. Researchers measured hepatic fat, plasma Alanine Aminotransferase (ALT), and Aspartate Aminotransferase (AST) levels to assess metabolic changes. Hepatic mitochondrial dynamics were examined using transmission electron microscopy and Western blot. Mitochondrial functions were evaluated through Quantitative Polymerase Chain Reaction (qPCR) and measurement of ATP content. In vitro, HepG2 cells were treated with palmitate (PA), β-hydroxybutyric acid (β-OHB), and/or the mitochondrial fusion inhibitor MFI8 to study mitochondrial morphology, function, and lipid deposition.

Results: KD feeding partially improved the MASLD phenotype and reduced Fission 1 protein (Fis1) and Dynamin-related protein 1 (Drp1) levels in the livers of MASLD mice. Additionally, KD ameliorated HFD-stimulated mitochondrial dysfunctions, as evidenced by elevated ATP levels and upregulation of key genes responsible for fatty-acid-oxidation. β-OHB mitigated PA-stimulated mitochondrial dysfunction and fission in HepG2 cells. Furthermore, β-OHB attenuated PA-stimulated lipid deposition, with this effect being counteracted by MFI8.

Conclusions: Our study suggests that a 2-week KD partially alleviates lipid deposition, restores mitochondrial dynamics balance, and improves mitochondrial dysfunctions in the livers of MASLD mice.