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Daily Treatment of Mice with Type 2 Diabetes with Adropin for Four Weeks Improves Glucolipid Profile, Reduces Hepatic Lipid Content and Restores Elevated Hepatic Enzymes in Serum
Adropin is a peptide hormone encoded by Energy Homeostasis Associated gene. Adropin modulates energy homeostasis and metabolism of lipids and carbohydrates. There is growing evidence demonstrating that adropin enhances insulin sensitivity and lowers hyperlipidemia in obese mice. The aim of this study was to investigate the effects of daily administration of adropin for four weeks in mice with experimentally induced type 2 diabetes (T2D). Adropin improved glucose control without modulating insulin sensitivity. Adropin reduced body weight, size of adipocytes, blood levels of triacylglycerol and cholesterol in T2D mice. T2D mice treated with adropin had lower liver mass, reduced hepatic content of triacylglycerol and cholesterol. Furthermore, adropin attenuated elevated blood levels of hepatic enzymes (ALT, AST, GGT and ALP) in T2D mice. In T2D mice, adropin increased the circulating adiponectin level. Adropin had no effects on circulating insulin and glucagon levels and did not alter pancreatic islets morphology. These results suggest that adropin improves glucose control, lipid metabolism and liver functions in T2D. In conjunction with reduced lipid content in hepatocytes, these results render adropin as an interesting candidate in therapy of T2D.
Spexin Promotes the Proliferation and Differentiation of C2C12 Cells In Vitro—The Effect of Exercise on SPX and SPX Receptor Expression in Skeletal Muscle In Vivo
SPX (spexin) and its receptors GalR2 and GalR3 (galanin receptor subtype 2 and galanin receptor subtype 3) play an important role in the regulation of lipid and carbohydrate metabolism in human and animal fat tissue. However, little is still known about the role of this peptide in the metabolism of muscle. The aim of this study was to determine the impact of SPX on the metabolism, proliferation and differentiation of the skeletal muscle cell line C2C12. Moreover, we determined the effect of exercise on the SPX transduction pathway in mice skeletal muscle. We found that increased SPX, acting via GalR2 and GalR3 receptors, and ERK1/2 phosphorylation stimulated the proliferation of C2C12 cells (p < 0.01). We also noted that SPX stimulated the differentiation of C2C12 by increasing mRNA and protein levels of differentiation markers Myh, myogenin and MyoD (p < 0.01). SPX consequently promoted myoblast fusion into the myotubule (p < 0.01). Moreover, we found that, in the first stage (after 2 days) of myocyte differentiation, GalR2 and GalR3 were involved, whereas in the last stage (day six), the effect of SPX was mediated by the GalR3 isoform. We also noted that exercise stimulated SPX and GalR2 expression in mice skeletal muscle as well as an increase in SPX concentration in blood serum. These new insights may contribute to a better understanding of the role of SPX in the metabolism of skeletal muscle.
LEAP2 in Physiology—A Narrative Review
Liver Enriched Antimicrobial Peptide 2 (LEAP2) is a fascinating peptide that has gained significant attention since its discovery in 2003. Initially identified as an antimicrobial peptide, LEAP2 has more recently been found to play a key role in the regulation of energy metabolism. One of the most notable functions of LEAP2 is its interaction with the ghrelin hormone, which is known for stimulating hunger. LEAP2 acts as an inhibitor of ghrelin, thereby reducing food intake and influencing energy balance. The physiological roles of LEAP2 extend beyond appetite suppression. Studies have shown that LEAP2 has an impact on insulin secretion, suggesting its potential involvement in glucose metabolism and possibly insulin sensitivity, which is crucial in managing conditions like type 2 diabetes. Moreover, LEAP2 levels appear to fluctuate based on factors such as gender, developmental stage, and even interventions like bariatric surgery, which is known for its role in managing obesity and diabetes. Given these findings, LEAP2 shows potential as a therapeutic target, particularly for addressing obesity and metabolic diseases such as type 2 diabetes. Its ability to influence food intake and energy balance makes it a promising candidate for further research into therapies aimed at weight regulation and glycemic control. In the future, LEAP2 could become an important agent in the development of treatments aimed at curbing obesity and its associated metabolic disorders.
Assessment of the effectiveness and safety of two-month oral supplementation with l-arginine depending on the type of lipid metabolism disorder in patients with atherosclerotic lower limb ischemia.
Mechanical properties of the mouse femur after treatment with diclofenac and running exercises
Purpose: The flexible properties of the bone are essential for the movement and protection of vital organs. The ability of a bone to resist fractures under the influence of large muscles and physical activity depends on its established mechanical properties. This article discusses how exercise such as treadmill running and taking non-steroidal anti-inflammatory drugs (NSAIDs), such as diclofenac, affect the musculoskeletal system by modifying the elastic and thermal properties of the left femur of a mouse. Methods: The research was conducted using 9-week-old C57BL/6J female mice. In order to investigate the elastic and thermal properties of bones, dynamic mechanical analysis (DMA) and differential scanning calorimetry (DSC) were performed. Results: The study of elastic properties, followed by in-depth statistical analysis, shows that taking diclofenac slightly reduces the elastic parameters of the bones under study. These changes are more pronounced in DSC studies, the shift of the observed endothermic peaks is on the order of several degrees with a simultaneous increase in the enthalpy of this process. Conclusions: The opposite effect of the applied factors – diclofenac and running – on the elastic properties of the bones of the examined mice was found. The external factors – running and diclofenac – modify the basic parameters of the endothermic process associated with the release of water.
From infancy to school age – a retrospective study of breastfeeding duration and early childhood health in a cohort of 6–7-year-olds
Effect of clinically uneventful carotid endarterectomy on pentraxin 3 concentration: relationships between cognitive functions, local inflammation, and duration of brain ischemia
IntroductionThe pentraxins are a superfamily of proteins characterized by the presence of a pentraxin domain at the C-terminal. One of them is pentraxin 3 (PTX3), which is of great interest to scientists, primarily due to its function as an endogenous modulator of the inflammatory response. Local inflammation is a common phenomenon during various types of surgery and procedures, and its causes, among others, are local ischemia or tissue irritation. One such procedure is carotid plaque removal by carotid endarterectomy (CEA), which is performed to reduce the risk of stroke.Material and methodsThe purpose of this study was to investigate the effect of CEA on PTX3 concentration and the relationship between cognitive functions and the duration of brain ischemia in patients. We evaluated the relationships using blood collected from patients undergoing CEA, the Mini-Mental State Examination (MMSE) questionnaire, and commercially available ELISA tests.ResultsResults: We found that the concentration of PTX3 increased after surgery (from 0.59 ± 0.11 to 1.29 ± 0.29 ng mL<sup>–1</sup>; <i>P</i> < 0.01). Also, a decrease in the MMSE score was observed 24 hours after the procedure (<i>P</i> < 0.01). However, just one month after the procedure, it significantly increased compared to the day of admission to the hospital (<i>P</i> < 0.01). Our results did not demonstrate any interactions between the tested parameters. It can be concluded that neither the changes in PTX3 concentration following the procedure nor the timing of these changes directly contribute to the temporary deterioration of cognitive functions observed after CEA.ConclusionsPTX3 increases independently of the duration of cerebral hypoxemia/ hypercapnia after clamping the carotid artery. This rise is an inflammatory marker that occurs independently within the central nervous system.
Genistein stimulates the viability and prevents myofibroblastic transformation in human trabecular meshwork cells stimulated by TGF-β
Neopterin Concentration in Umbilical Cord Blood as a Reflection of Maternal Insulin Resistance—A Pilot Study
Background/Objective: Insulin resistance (IR) during pregnancy, even in women with normal body mass index (BMI), may affect maternal and fetal metabolic and immune status. This study aimed to evaluate neopterin (NPT), leptin, insulin, and ghrelin concentrations in maternal blood (MB) and umbilical cord blood (CB) in normoglycemic women with and without IR, all with normal BMI. Methods: Peripheral and cord blood was collected from 36 Caucasian women with term, uncomplicated vaginal deliveries. The participants were classified into control (n = 16; age = 30.81 ± 4.875 years) and IR (n = 20; age = 31.95 ± 4.979 years) groups based on a professional medical diagnosis. Anthropometric parameters were recorded, and metabolic/hormonal markers were measured using ELISA and RIA. Results: NPT concentrations in CB were significantly higher in the IR group (p < 0.05), correlated positively with MB NPT levels (r = 0.3809, p < 0.05). A significantly higher concentration of both insulin and leptin was observed in the MB of women with IR compared to the control group (p < 0.0001), whereas in CB, only insulin concentration was significantly higher in the IR group than in healthy controls (p < 0.05). Ghrelin levels did not differ between the groups. Conclusions: Insulin resistance in non-obese pregnant women is associated with increased NPT concentration in CB, which may suggest fetal immune activation. However, defining the role of NTP as a metabolic “messenger” between mother and child requires further study.
The Effects of Protease Supplementation and Faba Bean Extrusion on Growth, Gastrointestinal Tract Physiology and Selected Blood Indices of Weaned Pigs
The aim of the study was to investigate how the extrusion of faba bean seeds (var. Albus) and/or the addition of protease to pigs’ diets affected the animals’ growth parameters, digestibility of nutrients, selected physiological parameters of the digestive tract, and biochemical blood parameters. A 28-day experiment was conducted on 32 pigs weighing 9 ± 0.2 kg. The animals were allocated to four treatments in a 2 × 2 factorial arrangement with the main effects of extrusion (raw or extruded) and effects of protease supplementation (0 and 0.05%). Extrusion reduced the levels of neutral detergent fibre, trypsin inhibitor, phytate-P, and resistant starch but did not improve the digestibility of protein and dry matter in faba bean seeds. The pigs’ growth performance, ileal digestibility, enzyme activity, and morphometric parameters of the ileum were not significantly affected by extrusion, except for a higher feed intake between the 15th and 28th day of the experiment. The protease supplementation gave comparable results as the diet without protease, except the feed conversion ratio (in the periods of 15–28th day and 0–28th day), which was higher than in the groups without protease. The extrusion and protease increased acetate and acetoacetate contents in the cecal digesta, but propionate, butyrate, and isovalerate concentrations in the digesta of the pigs in this group were lower. Thanks to protease supplementation, protein and oil levels in the diet were reduced, which cut the cost of feed mixtures. The extrusion and protease additive combined together did not improve the pigs’ growth performance in this experiment.
Effect of emulsifier and multicarbohydrase enzyme supplementation on performance and nutrient digestibility in broiler diets containing rapeseed meal
The Role of a High-Fat, High-Fructose Diet on Letrozole-Induced Polycystic Ovarian Syndrome in Prepubertal Mice
This study aims to investigate the effects of a high-fat, high-fructose (HF/HFr) diet on metabolic/endocrine dysregulations associated with letrozole (LET)-induced Polycystic Ovarian Syndrome (PCOS) in prepubertal female mice. Thirty-two prepubertal C57BL/6 mice were randomly divided into four groups of eight and implanted with LET or a placebo, with simultaneous administration of an HF/HFr/standard diet for five weeks. After sacrifice, the liver and blood were collected for selected biochemical analyses. The ovaries were taken for histopathological examination. The LET+HF/HFr group gained significantly more weight than the LET-treated mice. Both the LET+HF/HFr and the placebo-treated mice on the HF/HFr diet developed polycystic ovaries. Moreover the LET+HF/HFr group had significantly elevated testosterone levels, worsened lipid profile and indices of insulin sensitivity. In turn, the HF/HFr diet alone led to similar changes in the LET-treated group, except for the indices of insulin sensitivity. Hepatic steatosis also occurred in both HF/HFr groups. The LET-treated group did not develop endocrine or metabolic abnormalities, but polycystic ovaries were seen. Since the HF/HFr diet can cause substantial metabolic and reproductive dysregulation in both LET-treated and placebo mice, food items rich in simple sugar—particularly fructose—and saturated fat, which have the potential to lead to PCOS progression, should be eliminated from the diet of young females.
Ostarine-Induced Myogenic Differentiation in C2C12, L6, and Rat Muscles
Ostarine (also known as enobosarm or Gtx-024) belongs to the selective androgen receptor modulators (SARMs). It is a substance with an aryl-propionamide structure, classified as a non-steroidal compound that is not subjected to the typical steroid transformations of aromatization and reduction by α5 reductase. Despite ongoing research on ostarine, knowledge about it is still limited. Earlier studies indicated that ostarine may affect the metabolism of muscle tissue, but this mechanism has not been yet described. We aimed to investigate the effect of ostarine on the differentiation and metabolism of muscle. Using C2C12 and L6 cells, as well as muscles obtained from rats administered ostarine, we showed that ostarine stimulates C2C12 and L6 proliferation and cell viability and that this effect is mediated by androgen receptor (AR) and ERK1/2 kinase activation (p < 0.01). We also found that ostarine stimulates muscle cell differentiation by increasing myogenin, MyoD, and MyH expression in both types of cells (p < 0.01). Moreover, pharmacological blocking of AR inhibits the stimulatory effect of ostarine. We further demonstrated that 30 days of ostarine administration increases myogenin, MyoD, and MyH expression, as well as muscle mass, in rats (p < 0.01). Based on our research, we conclude that ostarine stimulates muscle tissue proliferation and differentiation via the androgen receptor.
Structural and biomechanical analysis of femurs from mice treated with diclofenac, miR-15b and miR-365
PurposeNonsteroidal anti-inflammatory drugs (NSAIDs) are used to treat pain, but they have side effects, including the inhibition of bone healing. Diclofenac (DF), a member of the NSAID group, affects bone health adversely. One potential approach to protect bones from the effects of NSAIDs involves the administration of short nucleic acids, such as microRNAs (miRNAs). This study aimed to determine whether two specific miRNAs, miR-15b and miR-365, could mitigate the effects of DF on bone.MethodsWe used the C57BL/6J mouse strain and the MC3T3-E1 pre-osteoblast cell line derived from this mouse strain. Female C57BL/6J mice were treated with DF and miR-15b or miR-365 mimics. After euthanising the mice, we analysed their femurs using micro-computed tomography (μCT) and dynamic mechanical analysis (DMA). In addition, we performed experiments in cultured MC3T3-E1 cells, which were transfected with either miR-15b or miR-365. We assessed the relative mRNA levels of osteoblast differentiation markers using real-time PCR.ResultsOur findings indicated that miR-15b and miR-365 were effective in reversing the detrimental effects of DF on bone mineral density. DF decreased the bone’s storage modulus (E’), while miR-15b and miR-365 ameliorated this effect. In the preosteoblast MC3T3-E1 cells, DF did not significantly regulate marker genes; however, the administration of miR-15b and miR-365 reduced the gene expression of Runx2, Alp, and Satb2.ConclusionsIn summary, the impact of DF on the structural and mechanical properties of bone was not mediated by gene regulation in osteoblasts. However, osteoblasts were responsive to the administration of miR-15b and miR-365.
MOTS-c modulates pancreatic islet function in rats and pigs in vitro
Abstract MOTS-c is a promising regulator of metabolism and energy homeostasis. While its effects have been studied in cell lines, our team aimed to investigate its influence on more complex structures—specifically, isolated pancreatic islets. We used two animal models: the rat, which is commonly studied, and the pig, which shares greater physiological similarities with humans. This study assessed the expression and secretion of insulin and glucagon, the expression of their receptors, cell viability, and cell death following MOTS-c treatment of the islets. Additionally, we examined how MOTS-c secretion is affected by different incubation media, such as the presence of free fatty acids, pancreatic hormones, and different glucose concentrations. The results indicate that MOTS-c impacts pancreatic islet physiology by, for example, reducing insulin and glucagon secretion and enhancing cell viability. Notably, the effects differed between the two species, which may be attributed to anatomical differences in their pancreatic islets or structural variations in rat and pig MOTS-c. These facts may lead to the conclusion that if MOTS-c may be helpful in human medicine, the pig model should be considered another valuable choice.
MOTS-c Impact on Muscle Cell Differentiation and Metabolism Across Fiber Types
Background/Aims: MOTS-c belongs to a group of mitochondrial peptides involved in metabolic processes in the body. This peptide has garnered increasing attention since its discovery in 2015 because of its potential to ameliorate metabolic parameters in animals with diabetes or insulin resistance. MOTS-c is involved in muscle metabolism; however, little is known about its role in fiber differentiation. Materials: We conducted a study to explore the effect of MOTS-c on cellular processes using the C2C12 and L6 cell lines, representing different metabolic types of muscle fibers. The research methods were real-time PCR, Western blot, and lipid accumulation measurement. Results: >Notably, our investigations revealed that MOTS-c increased the survival of C2C12 cells at doses of 10 and 100 nM (p<0.01) and stimulated the phosphorylation of extracellular signal-regulated kinase within 5 min of incubation (p<0.05). Remarkably, these effects were not observed in L6 cells; however, both cell lines showed a reduced rate of proliferation. Furthermore, MOTS-c promotes the differentiation of C2C12 cells by increasing the expression of muscle regulatory factors, but it does not produce such an effect in L6 cells. Additionally, cells were treated with physiological concentrations of free fatty acids and MOTS-c, unveiling an augmentation in lipid accumulation observed in L6 cells and a decrease in lipid accumulation in C2C12 cells. Conclusion: In conclusion, our findings have suggested a diverse response to MOTS-c depending on the type of muscle fibers, particularly in the domains of survival, cell differentiation, and lipid accumulation.
