Liver Glycogen Content Research Articles

Effect of Food Deprivation on Plasma Cortisol, Carbohydrate Metabolism, and Histomorphology in Clarias batrachus.

The nutritional status of fish is essential for its health, experimental studies, and aquaculture practices. The current study investigated the impact of food deprivation on biochemical parameters, histology of skin, gill, and kidney tissues, and ultrastructure of gills in Clarias batrachus. Fish were subjected to food deprivation for 2, 7, and 15 days resulting in (a) significant increase in plasma cortisol levels, (b) no significant changes in plasma osmolality and plasma glucose content, and (c) significant decrease in liver and muscle glycogen contents. A substantial damage was detected in skin, gill, and kidney tissues with histological alterations in a time-dependent manner. Skin tissue displayed melanomacrophage aggregation, excoriated epidermis and dermis. In gill tissue, epithelial lifting, edema, desquamation, deformed secondary lamellae, and lamellar hyperplasia were observed. Kidney tissue exhibited degenerated tubules, melanomacrophage aggregations, and shrunken renal tubule. Scanning electron microscopy revealed that food deprivation-induced marked presence of mucus, chloride cells, and pavement cells with well-defined microridges and microbridges following 2 days, opening of chloride cells was more prominent after 7 days, while more mucus secretion was observed after 15 days. After food deprivation, alterations in biochemical and histological parameters, and ultrastructural changes in target tissues reflect physiological and morphological disturbances in fish. The novelty of this study is that these parameters can be considered as biomarkers of feeding stress in fish and fish health and can provide important insights for better aquaculture practices.

Investigation of Pajanelia longifolia Leaf Extract for Antidiabetic Activity

Diabetes mellitus (DM) is a medical condition characterized by heightened levels of blood sugar, stemming from either inadequate production of insulin or an impaired response to insulin at the cellular level, whether due to a relative or absolute deficiency of the hormone. Traditional herbal remedies have a significant role in the treatment of DM. Pajanelia longifolia, known by the general population as Pajanelia or Tender wild jack has been a component of traditional herbal medicine in India and other Asian countries for the treatment of various ailments. The current research assessed the antidiabetic activity of Pajanelia longifolia leaf extract in streptozotocin (35 mg/kg, oral route) induced diabetic rats. The study utilized an in vivo streptozotocin induced diabetic model and an in vitro rat hemidiaphragm model for assessment of antidiabetic activity. Acute toxicity studies conducted on liposomes of Pajanelia longifolia leaf extract (2000 mg/kg body weight) proved the drug to be non-toxic. The effects of various doses (100, 200 and 400 mg/kg p.o.) of extract were assessed. Glimepiride (2 mg/kg) and insulin (0.25 IU/ml) were used as the standard drugs for in vivo and in vitro studies, respectively. The decrease in blood glucose levels and the elevation of muscle and liver glycogen content in diabetic rats induced by streptozotocin and the increased glucose uptake and glycogen content observed in in vitro rat hemidiaphragm technique proved that Pajanelia longifolia leaf extract has significant antidiabetic activity.

Histo-architectural and histochemical changes in the liver and intestine of Labeo rohita: integrative effect of water temperature and dietary protein level

This study aimed to study the histo-architectural and histochemical changes in the liver and intestine of Labeo rohita fingerlings due to the integrative effect of short-term exposure to higher temperature and dietary protein levels. Six hundred Labeo rohita fingerlings (average weight 6.78 ± 0.05 g) were distributed into 24 tanks, with 25 fingerlings in each tank. The tanks were divided into eight experimental groups, with three replicates for each tank. Half of the experimental groups were maintained at an ambient water temperature of 260C, while the other half were kept at 320C for one week and then shifted back to 260C for four weeks. The fingerlings were fed with either of four diets, each containing different protein levels of 20%, 30%, 40% or 45% protein. At the end of the experiment, the hepatosomatic index (HSI) and visceral index (VI) of the juveniles were increased with the increase in dietary protein level, however significantly lower HSI was recorded at 320C compared to 260C. Juveniles exposed to elevated temperature (320C) for one week registered significantly higher (p < 0.05) liver glycogen content compared to 260C. Amylase, protease, and alkaline phosphatase activity in the intestine of juveniles were significantly (p < 0.05) higher at elevated temperature (320C) and decreased after 4 weeks of decrease in temperature from elevated temperature (320C) to ambient temperature (260C). The 45% CP fed group at 260C showed mildly desquamated mucosa in the liver whereas mucosa was found absent at 320C. Marked loss of mucosa was found in the intestine of L. rohita fed with 45% dietary protein after five weeks either at 260C or 320C. Overall it concludes that the dietary protein level and water temperature interactions are more effective in maintaining the histo-architectural structure of the liver and intestine, which responds to increased digestive enzyme activity.

Jingfang Granule promotes the tricarboxylic acid cycle to improve chronic fatigue syndrome by increasing the expression of Idh1 and Idh2.

Chronic fatigue syndrome (CFS), as a complex, multisystemic, and multisystemic disorder affecting multiple organs and systems, often accompanies by symptoms such as post-exercise discomfort, sleep disorders, cognitive difficulties, and orthostatic intolerance. Jingfang Granule (JFG) is a traditional Chinese medicine that have significant protective effects on CFS, but the mechanism is still vague. This study was designed to evaluate the protective mechanism of JFG on mice with CFS. The combined stimuli method was used to establish the mice CFS model, and JFG was orally administered. The body weight, exhaustion swimming training and tail suspension test were assayed every 7 days to evaluate the improvement of JFG on CFS. Lactic acid, adenosine triphosphate (ATP), malondialdehyde (MDA), superoxide dismutase (SOD), reactive oxygen species (ROS), IL-1β, TNF-α, IL-6 in serum and liver glycogen, muscle glycogen in muscle were analyzed. Transmission electron microscopy was used to detect mitochondrial morphology. The regulatory networks were investigated by proteomics and central carbon metabolomics, which were verified by Western blot. JFG reversed the loss of weight and reduce of exhaust swimming time (P<0.05) induced by CFS in mice, and increased the tail suspension time (P<0.05), indicating that JFG has an improving effect on CFS. Meanwhile, JFG increased the spleen index (P<0.05), decreased the thymus index (P<0.05) and cardiac index (P<0.05), inhibited the secretion of Lactic acid (P<0.05), and increased the content of liver glycogen (P<0.05), muscle glycogen (P<0.05), and ATP (P<0.05), and improved mitochondrial morphology in mice with CFS. JFG also inhibited the release of TNF-α (P<0.05), IL-1β (P<0.05) and IL-6 (P<0.05) in serum by inhibiting TLR4/NF-κB signaling pathway and NLRP3 inflammasome signaling pathway, and inhibited oxidative stress by activating Nrf2/HO-1/NQO1 axis. Integrated central carbon metabolomics, proteomics and Western blot showed that JFG intervened in CFS by increasing the expression of Idh1 (P<0.05) and Idh2 (P<0.01) to promote tricarboxylic acid (TCA) cycle. This study confirmed that JFG promoted the TCA cycle by increasing the expression of Idh1 and Idh2, and then inhibited inflammation and oxidative stress to prevent CFS injury, which provided a potential drug candidate for CFS treatment.

Ozone treatment regulated the anti-exercise fatigue effect of fresh-cut pitaya polyphenol extracts.

The anti-exercise fatigue effect of plant polyphenols is closely related to the content, composition, and extractability of phenolic substances. According to our previous findings, ozone treatment significantly affected the biological effects of fresh-cut pitaya polyphenols. Therefore, this study used C57BL/6 J mice to explore the regulatory mechanism of ozone treatment on the anti-exercise fatigue effect of fresh-cut pitaya polyphenol extract. The result showed that fresh-cut pitaya polyphenols treated with ozone (OP) have a better effect. Compared with the untreated group, the exhaustion time of the OP group was 11.86% longer, the total antioxidant capacity was 54.17% higher, the MDA content was 32.8% lower, and the liver glycogen content was 85.71% higher. The OP group also better regulated substrate metabolism, protecting muscle and visceral weight. The results of RT-PCR were consistent with the results of network pharmacology, and the expression of PI3K and AKT was activated, while SRC and STAT3 were down-regulated. Furthermore, pitaya polyphenols have been demonstrated to exert anti-fatigue effects by increasing the diversity of gut microbiota species. In summary, ozone treatment is a feasible way to improve the nutrition of polyphenols.

Maternal under-nutrition during pregnancy alters the molecular response to over-nutrition in multiple organs and tissues in nonhuman primate juvenile offspring.

Previous studies in rodents suggest that mismatch between fetal and postnatal nutrition predisposes individuals to metabolic diseases. We hypothesized that in nonhuman primates (NHP), fetal programming of maternal undernutrition (MUN) persists postnatally with a dietary mismatch altering metabolic molecular systems that precede standard clinical measures. We used unbiased molecular approaches to examine response to a high fat, high-carbohydrate diet plus sugar drink (HFCS) challenge in NHP juvenile offspring of MUN pregnancies compared with controls (CON). Pregnant baboons were fed ad libitum (CON) or 30% calorie reduction from 0.16 gestation through lactation; weaned offspring were fed chow ad libitum. MUN offspring were growth restricted at birth. Liver, omental fat, and skeletal muscle gene expression, and liver glycogen, muscle mitochondria, and fat cell size were quantified. Before challenge, MUN offspring had lower body mass index (BMI) and liver glycogen, and consumed more sugar drink than CON. After HFCS challenge, MUN and CON BMIs were similar. Molecular analyses showed HFCS response differences between CON and MUN for muscle and liver, including hepatic splicing and unfolded protein response. Altered liver signaling pathways and glycogen content between MUN and CON at baseline indicate in utero programming persists in MUN juveniles. MUN catchup growth during consumption of HFCS suggests increased risk of obesity, diabetes, and cardiovascular disease. Greater sugar drink consumption in MUN demonstrates altered appetitive drive due to programming. Differences in blood leptin, liver glycogen, and tissue-specific molecular response to HFCS suggest MUN significantly impacts juvenile offspring ability to manage an energy rich diet.

Anti-fatigue effect of pigeon meat hydrolysate on exercise mice and its underlying mechanism: Related to oxidative stress and energy metabolism

With the acceleration of the pace in modern society, fatigue caused by high-intensity physical work, long-term heavy mental work and lack of sleep has become a widespread and noticeable health problem. In this study, pigeon meat hydrolysate (PMH) with good antioxidant activity was prepared and the anti-fatigue effects of fractions in PMH with different molecular weights (MW) on exercise mice and the underlying mechanism were investigated. Results showed that mice gavaged with PMH and its fractions exhibited improved exhaustive swimming time when compared to the Control, with fraction at MW 1–5 kDa (PP2) showed the highest improvement. Meanwhile, PP2 decreased the levels of blood lactate acid (BLA) and blood urea nitrogen (BUN), and increased the contents of muscle and liver glycogen. And the activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase in myocyte of mice were significantly enhanced, with the outflow of creatine kinase (CK) reduced. PP2 also exhibited significant antioxidant activity by increasing the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and reducing the production of malondialdehyde (MDA), especially at relative higher dosages (M-PP2 and H-PP2). Metabolomics study indicated that the differential metabolites between PP2 and the Control group in liver tissues of mice were mainly related to the energy metabolism and central nervous system regulation pathways. All these results demonstrated that PP2 fraction in PMH at a dosage higher than 0.5 mg/g of mice body weight could significantly enhance the exercise endurance of mice and exert excellent anti-fatigue ability via alleviating oxidative stress and modulating energy metabolism in mice.

Knockout of the Muscle-Specific E3 Ligase MuRF1 Affects Liver Lipid Metabolism upon Dexamethasone Treatment in Mice.

In order to preserve muscle mass during catabolic states, investigators are actively searching for a specific inhibitor of MuRF1, the only known E3 ligase that can target muscle contractile proteins for their degradation. However, what would be the consequences of such inhibitors on other organs, both in the short and long term? Indeed, skeletal muscles can provide amino acids for liver gluconeogenesis, which is a crucial adaptation for maintaining glucose homeostasis upon elevated energy demands (e.g., during prolonged starvation). Comparing 3-month-old wild-type and MuRF1-KO mice, we measured tissue weights, liver glycogen, lipid and protein content, and liver biochemical composition using Fourier transform infrared (FTIR) spectrometry in control animals and in dexamethasone (Dex)-treated animals. Dex induces a catabolic situation with muscle atrophy and lipid deposits in the liver. In response to Dex treatment, liver glycogen, lipid, and protein content increased in wild type (WT) and MuRF1-KO mice. We found that MuRF1 deletion differentially affected organ weights, the liver of KO mice being hypertrophied upon Dex treatment when compared to WT mice. Upon Dex treatment, muscle mass was preserved in MuRF1-KO mice, and by contrast, liver lipid content increased more in these animals than in WT mice. PLS-DA analysis of FTIR showed that the levels of 13 markers were significantly altered in KO vs WT mice, witnessing profound alterations of lipid, protein, and glycogen content in the liver due to the absence of MuRF1. Using Nile red and oil red lipid staining, we also found that both membrane-linked lipids and intracellular lipid droplets were altered due to the absence of MuRF1. Altogether, it seems that when the liver is deprived of the possibility of obtaining amino acids from muscle upon Dex treatment, there is a concomitant increase in tissue weight and anabolic activity.

Cardiac corin and atrial natriuretic peptide regulate liver glycogen metabolism and glucose homeostasis

BackgroundCardiovascular function and metabolic homeostasis are closely linked, but the underlying mechanisms are not fully understood. Corin is a protease that activates atrial natriuretic peptide (ANP), an essential hormone for normal blood pressure and cardiac function. The goal of this study is to investigate a potential corin and ANP function in regulating liver glycogen metabolism and glucose homeostasis.MethodsLiver glycogen and blood glucose levels were analyzed in Corin or Nppa (encoding ANP) knockout (KO) mice. ANP signaling was examined in livers from Corin and Nppa KO mice and in cultured human and mouse hepatocytes by western blotting.ResultsWe found that Corin and Nppa KO mice had reduced liver glycogen contents and increased blood glucose levels. By analyzing conditional KO mice lacking either cardiac or renal Corin, we showed that cardiac corin and ANP act in an endocrine manner to enhance cGMP-protein kinase G (PKG)-AKT-GSK3 signaling in hepatocytes. In cultured hepatocytes, ANP treatment stimulated PKG signaling, glucose uptake, and glycogen production, which could be blocked by small molecule PKG and AKT inhibitors.ConclusionsOur results indicate that corin and ANP are important regulators in liver glycogen metabolism and glucose homeostasis, suggesting that defects in the corin and ANP pathway may contribute to both cardiovascular and metabolic diseases.

Long-chain perfluoroalkylether carboxylic acids PFO5DoA and PFO4DA alter glucose, bile acid, and thyroid hormone homeostasis in fetal rats from 5-day maternal oral exposure

Chemical monitoring studies in North Carolina, USA and Shandong, China have reported detections of perfluoroalkylether carboxylic acids of increasing chain length with ether bonds between each fluorinated carbon. Despite detection there is limited hazard data available to inform risk assessment. Here, we exposed pregnant Sprague-Dawley rats to two of these compounds, perfluoro-3,5,7,9-butaoxadecanoic acid (PFO4DA) and perfluoro-3,5,7,9,11-pentaoxadodecanoic acid (PFO5DoA), from gestation days 18–22 across a series of doses (0.3–62.5 mg/kg/d) via oral gavage. PFO5DoA was acutely toxic to rat dams and fetuses at the top two doses (30 and 62.5 mg/kg), while PFO4DA did not cause acute toxicity at any doses tested. PFO5DoA significantly increased maternal liver weight (≥3 mg/kg; 28% increase at 10 mg/kg) while PFO4DA did not affect maternal liver weight up to 62.5 mg/kg. PFO4DA and PFO5DoA both significantly reduced serum total thyroxine in maternal (≥10 mg/kg for both) and fetal (≥1 mg/kg) rats. Both compounds significantly reduced fetal liver glycogen concentrations, increased fetal serum total bile acids, and altered expression levels of multiple genes associated with glucose metabolism in the fetal liver. Serum concentrations of PFO5DoA were higher than PFO4DA in both rat dams and fetuses at equivalent maternal oral doses indicating greater accumulation. Dose response modelling of several fetal endpoints as a function of serum molar concentration indicates PFO5DoA was ∼3-4-fold more potent than PFO4DA. PFO5DoA and PFO4DA produced maternal and fetal toxicity from short-term oral maternal exposure indicating need for additional toxicity data to evaluate potential human health risks.

Propylthiouracil thyroid manipulation positively affects the metabolic adaptability of primiparous dairy cows to early lactation requirements

The study examined effects of thyroid manipulation with propylthiouracil (PTU) on the metabolic adaptability of transitional dairy cows to early lactation. The study included 30 primiparous Holstein-Friesian cows, which were divided into two groups: PTU+ (n = 15; received orally 4 mg/kg PTU during 20 days before expected calving) and PTU− (n = 15; did not receive orally PTU). Blood was sampled from each cow consecutively from − 20, − 17, − 13, − 5, − 4, − 3, − 2, and − 1 days before the expected term of calving, calving day (0), and + 1, + 2, + 3, + 4, + 5, + 10, + 15, + 30 and + 60 days after the calving to measure thyroid stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), insulin, glucose, beta-hydroxybutyrate (BHB), bilirubin, total protein and albumin concentrations. Liver samples were biopsied at −7 ± 2 and +7 day relative to calving from both groups of cows to determine deiodinase (DIO) expressions and fat and glycogen content. Additionally, milk yield was monitored during the first 60 days of lactation. PTU successfully induced thyroid suppression by significantly reducing T3 and T4 concentrations and hepatic DIO1 expressions and caused PTU+ cows to have significantly higher insulin and glucose concentration in the precalving period. After calving, PTU+ cows had higher insulin and glucose concentration, liver glycogen content and overall milk production, lower BHB concentration, BCS loss, and liver fat deposits. Accordingly, cows treated with PTU have a more favourable energy balance and metabolic adaptation to early lactation.

Antidiabetic Effect of Bifidobacterium animalis TISTR 2591 in a Rat Model of Type 2 Diabetes.

This study investigated the beneficial effects of probiotic Bifidobacterium animalis TISTR 2591 on the regulation of blood glucose and its possible mechanisms in a rat model of type 2 diabetes. The type 2 diabetic-Sprague Dawley rats were established by the combination of a high-fat diet and a low dose of streptozotocin. After 4weeks of treatment with 2 × 108CFU/ml of B. animalis TISTR 2591, fasting blood glucose (FBG), oral glucose tolerance, serum insulin, and pancreatic and hepatic histopathology were determined. Liver lipid accumulation, glycogen content, and gluconeogenic protein expression were evaluated. Oxidative stress and inflammatory status were determined. B. animalis TISTR 2591 significantly reduced FBG levels and improved glucose tolerance and serum insulin in the diabetic rats. Structural damage of the pancreas and liver was ameliorated in the B. animalis TISTR 2591-treated diabetic rats. In addition, significant decreases in hepatic fat accumulation, glycogen content, and phosphoenolpyruvate carboxykinase-1 protein expression were found in the diabetic rats treated with B. animalis TISTR 2591. The diabetic rats showed a significant reduction of inflammation following B. animalis TISTR 2591 supplementation, as demonstrated by decreasing hepatic NF-κB protein expression and serum and liver TNF-α levels. The B. animalis TISTR 2591 significantly decreased MDA levels and increased antioxidant SOD and GPx activities in the diabetic rats. In conclusion, B. animalis TISTR 2591 was shown to be effective in controlling glucose homeostasis and improving glucose tolerance in the diabetic rats. These beneficial activities were attributed to reducing oxidative and inflammatory status and modulating hepatic glucose metabolism.

Early metabolic and transcriptomic regulation in rainbow trout (Oncorhynchus mykiss) liver by 11-deoxycorticosterone through two corticosteroid receptors pathways

Cortisol hormone is considered the main corticosteroid in fish stress, acting through glucocorticoid (GR) or mineralocorticoid (MR) receptor. The 11-deoxycorticosterone (DOC) corticosteroid is also secreted during stress and could complement the cortisol effects, but this still not fully understood. Hence, we evaluated the early transcriptomic response of rainbow trout (Oncorhynchus mykiss) liver by DOC through GR or MR. Thirty juvenile trout were pretreated with an inhibitor of endogenous cortisol synthesis (metyrapone) by intraperitoneal injection in presence or absence of GR (mifepristone) and MR (eplerenone) pharmacological antagonists for one hour. Then, fish were treated with a physiological DOC dose or vehicle (DMSO-PBS1X as control) for three hours (n = 5 per group). We measured several metabolic parameters in plasma, together with the liver glycogen content. Additionally, we constructed cDNA libraries from liver of each group, sequenced by HiseqX Illumina technology and then analyzed by RNA-seq. Plasma pyruvate and cholesterol levels decreased in DOC-administered fish and only reversed by eplerenone. Meanwhile, DOC increased liver glycogen contents depending on both corticosteroid receptor pathways. RNA-seq analysis revealed differential expressed transcripts induced by DOC through GR (448) and MR (1901). The enriched biological processes to both were mainly related to stress response, protein metabolism, innate immune response and carbohydrates metabolism. Finally, we selected sixteen genes from enriched biological process for qPCR validation, presenting a high Pearson correlation (0.8734 average). These results describe novel physiological effects of DOC related to early metabolic and transcriptomic responses in fish liver and differentially modulated by MR and GR.

Glycogenic hepatopathy associated with hepatic steatosis in type 1 diabetes

AimsGlycogenic hepatopathy is associated with significant psychosocial consequences and health costs. Metabolic Dysfunction-Associated Steatotic Liver Disease and glycogenic hepatopathy are frequently confused as “fatty liver” when seen on ultrasonography. We wished to examine liver fat and glycogen content in groups defined based on metabolic and liver disease phenotypes. MethodsThis case-control study undertaken in a tertiary hospital used nuclear proton magnetic resonance spectroscopy (1H-MRS) to examine liver fat and glycogen content in five clinical groups, each containing five participants: 1. type 1 diabetes with glycogenic hepatopathy, 2. satisfactorily controlled type 1 diabetes with no liver disease, 3. poorly controlled type 1 diabetes without liver disease, 4. a control group of body mass index- and age-matched individuals without diabetes or liver disease, and 5. hepatic steatosis. ResultsFat content was highest in the hepatic steatosis (median 15.4 %, IQR 10.0–19.3) and glycogenic hepatopathy (median 6.5 %, IQR 4.5–9.1) groups and compared to both of these groups was lower in the control group (median 1.0 %, IQR 0.7–1.1, p 0.002 and 0.022), the T1DM group with satisfactory control (median 0.3 %, IQR 0.2–0.6, p < 0.001 and <0.001), and the T1DM group with poor control without liver disease (median 1.1 %, IQR 0.9–1.1, p 0.001 and 0.012).No participants from the type 1 diabetes poor control, type 1 diabetes satisfactory control or the no diabetes groups had 1H-MRS-diagnosed hepatic steatosis.1H-MRS glycogen content could not be interpreted in the majority of those with glycogenic hepatopathy because of interference from the fat signal. ConclusionsIn cases diagnosed with glycogenic hepatopathy there may be significant concomitant fat accumulation, compounding the already elevated cardiovascular risk in this cohort.The technique of 1H-MRS has not been demonstrated to be useful for diagnosing glycogenic hepatopathy.

Axin interactor, dorsalization-associated (AIDA) protein promotes appetite and regulates hepatic glycolipid metabolism in Schizothorax prenanti

Axin interactor, dorsalization-associated (AIDA) is a protein that interacts with Axin and involved in the regulation of embryonic development, intestinal fat absorption, and adaptive thermogenesis in brown adipose tissue. However, the roles of AIDA in feeding behavior and hepatic glycolipid metabolism in the fish remain uncovered. In this study, the AIDA gene of Schizothorax prenanti (S. prenanti) was cloned and the recombination AIDA protein of S. prenanti was obtained using a prokaryotic expression system. The highest expression level of the AIDA gene was detected in the hypothalamus, followed by the cerebral cortex, liver, muscle, and heart. Fasting induced the expression level of AIDA gene in the liver, cerebral cortex, and hypothalamus, but refeeding attenuated the AIDA expression. Furthermore, the recombinant AIDA protein (200 ng/g BW) i.c.v. injection increased the food intake of S. prenanti by increasing the expression levels of orexigenic factors (AgRP and Ghrelin) and decreasing the expression of anorexigenic factors (Cart, CCK, and Leptin). In addition, the i.p. injection of recombinant AIDA protein significantly decreased the glucose, TC, and TG contents in plasma and reduced the glycogen and TG contents in liver. These results demonstrate that AIDA protein increases appetite and regulates hepatic glycolipid metabolic processes in S. prenanti.

Liver Biopsy Technique for Analysis of Hepatic Content during Pregnancy and Early Lactation in Dairy Goats.

Biopsy techniques in dairy goats are currently limited. This study aimed to describe a liver biopsy technique in dairy goats and to evaluate liver triglyceride levels and glycogen content. Sixty-nine dairy goats in the final stage of pregnancy and early lactation period were selected. Fifty goats were selected randomly for hepatic biopsy (HB) according to gestational period and were characterized according to fetus number (single: n = 16, multiple: n = 34), supplementation with propylene glycol (diet: n = 23, diet+PG: n = 27), and milk production levels (high: 3.0 ± 0.4 L/day, n = 15; low: 1.4 ± 0.4 L/day, n = 26). Liver tissue samples were obtained through biopsy on days -30, -20, -15, -10, -5, and 15 days after calving. Hepatic triglyceride and glycogen were quantified. The results were analyzed using the F-test at a 5% significance level and a comparison of means using the Tukey test. The liver biopsies did not influence dry matter intake, body weight, or milk yield. Hepatic glycogen concentration was lower 15 days after calving than it was prior to calving, except on day -20. Goats that generated high levels of milk production had lower triglyceride levels than goats that generated low levels of milk production. The biopsy technique is a safe method for obtaining tissue and evaluating liver content in dairy goats. The milk production level and days relative to parturition influence the hepatic triglyceride and glycogen content in dairy goats.

Characterizing and identifying of miRNAs involved in berberine modulating glucose metabolism of Megalobrama amblycephala.

The present study, as one part of a larger project that aimed to investigate the effects of dietary berberine (BBR) on fish growth and glucose regulation, mainly focused on whether miRNAs involve in BBR's modulation of glucose metabolism in fish. Blunt snout bream Megalobrama amblycephala (average weight of 20.36 ± 1.44g) were exposed to the control diet (NCD, 30% carbohydrate), the high-carbohydrate diet (HCD, 43% carbohydrate) and the berberine diet (HCB, HCD supplemented with 50mg/kg BBR). After 10weeks' feeding trial, intraperitoneal injection of glucose was conducted, and then, the plasma and liver were sampled at 0h, 1h, 2h, 6h, and 12h. The results showed the plasma glucose levels in all groups rose sharply and peaked at 1h after glucose injection. Unlike the NCD and HCB groups, the plasma glucose in the HCD group did not decrease after 1h, while remained high level until at 2h. The NCD group significantly increased liver glycogen content at times 0-2h compared to the other two groups and then liver glycogen decreased sharply until at times 6-12h. To investigate the role of BBR that may cause the changes in plasma glucose and liver glycogen, miRNA high-throughput sequencing was performed on three groups of liver tissues at 2h time point. Eventually, 20 and 12 differentially expressed miRNAs (DEMs) were obtained in HCD vs NCD and HCB vs HCD, respectively. Through function analyzing, we found that HCD may affect liver metabolism under glucose loading through the NF-κB pathway; and miRNAs regulated by BBR mainly play roles in adipocyte lipolysis, niacin and nicotinamide metabolism, and amino acid transmembrane transport. In the functional exploration of newly discovered novel:Chr12_18892, we found its target gene, adenylate cyclase 3 (adcy3), was widely involved in lipid decomposition, amino acid metabolism, and other pathways. Furthermore, a targeting relationship of novel:Chr12_18892 and adcy3 was confirmed by double luciferase assay. Thus, BBR may promote novel:Chr12_18892 to regulate the expression of adcy3 and participate in glucose metabolism.

Systematical Investigation on Anti-Fatigue Function and Underlying Mechanism of High Fischer Ratio Oligopeptides from Antarctic Krill on Exercise-Induced Fatigue in Mice.

High Fischer ratio oligopeptides (HFOs) have a variety of biological activities, but their mechanisms of action for anti-fatigue are less systematically studied at present. This study aimed to systematically evaluate the anti-fatigue efficacy of HFOs from Antarctic krill (HFOs-AK) and explore its mechanism of action through establishing the fatigue model of endurance swimming in mice. Therefore, according to the comparison with the endurance swimming model group, HFOs-AK were able to dose-dependently prolong the endurance swimming time, reduce the levels of the metabolites (lactic acid, blood urea nitrogen, and blood ammonia), increase the content of blood glucose, muscle glycogen, and liver glycogen, reduce lactate dehydrogenase and creatine kinase extravasation, and protect muscle tissue from damage in the endurance swimming mice. HFOs-AK were shown to enhance Na+-K+-ATPase and Ca2+-Mg2+-ATPase activities and increase ATP content in muscle tissue. Meanwhile, HFOs-AK also showed significantly antioxidant ability by increasing the activities of superoxide dismutase and glutathione peroxidase in the liver and decreasing the level of malondialdehyde. Further studies showed that HFOs-AK could regulate the body's energy metabolism and thus exert its anti-fatigue effects by activating the AMPK signaling pathway and up-regulating the expression of p-AMPK and PGC-α proteins. Therefore, HFOs-AK can be used as an auxiliary functional dietary molecules to exert its good anti-fatigue activity and be applied to anti-fatigue functional foods.

Hypoglycemic Action of Glycocar on Insulin and Glucose Metabolism In Vivo

Background: Diabetes mellitus, particularly type 2, presents a growing global health challenge, with an estimated 700 million people expected to be affected by 2045. The disease is characterized by insulin resistance and impaired insulin secretion, necessitating effective treatments. This study aimed to explore the hypoglycemic mechanisms of Glykokar, a herbal formulation, in rats with alloxan-induced diabetes. The objective of this study was to investigate the hypoglycemic mechanisms of Glykokar, a herbal formulation. Methods: Eighteen rats with alloxan-induced diabetes were divided into groups receiving Glykokar at doses of 50 mg/kg or 100 mg/kg, and a control group receiving saline. The study measured the effects of Glykokar on C-peptide levels, glycogen content in liver and muscle, and the activity of hexokinase and phosphorylase enzymes over 7 and 14 days. Results: Results demonstrated that Glykokar significantly increased C-peptide levels, with the 100 mg/kg dose showing the greatest effect, enhancing C-peptide by 87.5% on day 14 compared to controls. Glycogen content in liver and muscle tissues was also elevated, particularly at the 100 mg/kg dose, which increased liver glycogen by 86% and muscle glycogen by 50%. Enzyme activity studies revealed that Glykokar reduced phosphorylase activity in diabetic muscle tissue and significantly boosted hexokinase and glucokinase activities, with the highest effects seen at the 100 mg/kg dose. Conclusion: The findings suggest that Glykokar’s hypoglycemic action is mediated through enhanced glucose metabolism in tissues, driven by increased enzymatic activity and glycogen storage. This study provides evidence for the potential of Glykokar as a therapeutic agent in managing hyperglycemia by improving glucose utilization and insulin secretion.

A non-antibiotic erythromycin derivative improves muscle endurance by regulating endogenous anti-fatigue protein orosomucoid in mice.

At present, there are no official approved drugs for improving muscle endurance. Our previous research found acute phase protein orosomucoid (ORM) is an endogenous anti-fatigue protein, and macrolides antibiotics erythromycin can elevate ORM level to increase muscle bioenergetics and endurance parameters. Here, we further designed, synthesized and screened a new erythromycin derivative named HMS-01, which lost its antibacterial activity in vitro and in vivo. Data showed that HMS-01 could time- and dose-dependently prolong mice forced-swimming time and running time, and improve fatigue index in isolated soleus muscle. Moreover, HMS-01 treatment could increase the glycogen content, mitochondria number and function in liver and skeletal muscle, as well as ORM level in these tissues and sera. In Orm-deficient mice, the anti-fatigue and glycogen-elevation activity of HMS-01 disappeared. Therefore, HMS-01 might act as a promising small molecule drug targeting ORM to enhance muscle endurance.