Hepatic Glycogen Levels Research Articles

Use of sodium butyrate in the feeding of Arapaima gigas (Schinz, 1822) juvenile

The objective of this study was to evaluate the sodium butyrate in the feeding of pirarucu juveniles, Arapaima gigas. Seventy - five juveniles of A. gigas (132.07 ± 3.12 g) were distributed in fifteen 310 L- tanks with constant aeration, filtration system and closed water recirculation. A completely randomized design the experiment, with four treatments including sodium butyrate (98%) in the diets (BS0 = control diet without sodium butyrate, BS1 = 0.5 g kg−1, BS2 = 1.0 g kg−1, BS3 = 1.5 g kg−1, BS4 = 2.0 g kg−1) with three replicates, and five juvenile treatment−1. The fish were fed three times day−1 (8, 12 and 16 h), until apparent satiety, for 45 days. Water quality parameters such as temperature, pH, dissolved oxygen and ammonia were monitored three times in the week. The growth parameters as weight gain, mean feed consumption, feed conversion ratio, specific growth rate, and survival were evaluated. It was performed chemical analysis of the whole body to establish dry matter, crude protein, ethereal extract, ash and gross energy. The hepatosomatic index and viscerosomatic index of juveniles also were evaluated. Histological sections of the intestine showed greater villous height and enzymatic activity of amylase, lipase and nonspecific alkaline protease. The blood plasma of juveniles was analyzed, as the hematocrit, total plasma protein concentration, triglyceride, glucose, and cholesterol. The inclusion of 1.17 g kg−1 of sodium butyrate in diets for A. gigas juveniles improves the growth parameters. This level favors feed conversion ratio increased intestinal villous height, without interfering in the blood parameters, and promote the adaptation of the enzymatic activity of amylase, lipase and nonspecific alkaline protease. Furthermore, it reduces the activity of aspartate aminotransferase and increases hepatic glycogen levels, making the animals more resistant to potentially stressful conditions in the growing environment.

The Antidiabetic and Antinephritic Activities of Auricularia cornea (An Albino Mutant Strain) via Modulation of Oxidative Stress in the db/db Mice

This study first systematically analyzed the constituents of an albino mutant strain of Auricularia cornea (AU). After 8 weeks of continuous treatment with metformin (Met) (0.1 g/kg) and AU (0.1 and 0.4 g/kg), db/db mice showed hypoglycemic functioning, indicated by reduced bodyweight, food intake, plasma glucose, serum levels of glycated hemoglobin A1c and glucagon, hepatic levels of phosphoenolpyruvate carboxykinase and lucose-6-phosphatasem, and increased serum levels of insulin. The effect of hypolipidemic functions were indicated by suppressed levels of total cholesterol and triglyceride, and enhanced levels of hepatic glycogen and high-density lipoprotein cholesterol. The renal protective effect of AU was confirmed by the protection in renal structures and the regulation of potential indicators of nephropathy. The anti-oxidative and anti-inflammatory effects of AU were verified by a cytokine array combined with an enzyme-linked immunosorbent assay. AU decreased the expression of protein kinase C α and β2 and phosphor-nuclear factor-κB, and enhanced the expression of catalase, nuclear respiratory factor 2 (Nrf2), manganese superoxide dismutase 2, heme oxygenase-1 and−2, heat shock protein 27 (HSP27), HSP60, and HSP70 in the kidneys of db/db mice. The results confirmed that AU's anti-diabetic and anti-nephritic effects are related to its modulation on oxidative stress.

2,3,7,8-Tetrachlorodibenzo-p-dioxin abolishes circadian regulation of hepatic metabolic activity in mice

Aryl hydrocarbon receptor (AhR) activation is reported to alter the hepatic expression of circadian clock regulators, however the impact on clock-controlled metabolism has not been thoroughly investigated. This study examines the effects of AhR activation on hepatic transcriptome and metabolome rhythmicity in male C57BL/6 mice orally gavaged with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) every 4 days for 28 days. TCDD diminished the rhythmicity of several core clock regulators (e.g. Arntl, Clock, Nr1d1, Per1, Cry1, Nfil3) in a dose-dependent manner, involving either a ≥ 3.3-fold suppression in amplitude or complete loss of oscillation. Accordingly, protein levels (ARNTL, REV-ERBα, NFIL3) and genomic binding (ARNTL) of select regulators were reduced and arrhythmic following treatment. As a result, the oscillating expression of 99.6% of 5,636 clock-controlled hepatic genes was abolished including genes associated with the metabolism of lipids, glucose/glycogen, and heme. For example, TCDD flattened expression of the rate-limiting enzymes in both gluconeogenesis (Pck1) and glycogenesis (Gys2), consistent with the depletion and loss of rhythmicity in hepatic glycogen levels. Examination of polar hepatic extracts by untargeted mass spectrometry revealed that virtually all oscillating metabolites lost rhythmicity following treatment. Collectively, these results suggest TCDD disrupted circadian regulation of hepatic metabolism, altering metabolic efficiency and energy storage.

Antidiabetic and Haematological Effects of Chrysophyllum albidum Supplemented Diet on Streptozotocin Induced Diabetic Rats

Background: The use of food in the management of diseases is an established art of science. It is essentially important in the management of chronic diseases such as diabetes mellitus where cure is not certain.
 Objective: This study investigated the anti-diabetic and heamatological effects of Chrysophyllum albidum fruit-skin (CAFS) supplemented diet on streptozotocin induced diabetic rats.
 Methods: Diabetes mellitus was induced by a single intraperitoneal injection of 50 mg/kg streptozotocin (STZ) and 70g/kg CAFS supplemented diet was used on STZ-induced diabetic rats to test its antidiabetic efficacy with some biochemical parameters and histological evaluation of liver and pancreatic tissues for a treatment period of twenty-eight days.
 Results: The diabetic untreated rats exhibited hyperglycaemia accompanied with increases in glycosylated haemoglobin, plasma and liver lipid profile except high density lipoprotein-cholesterol (HDL-c) and white blood cell count while decreasing the body weight, insulin, hepatic glycogen and red blood cell levels. CAFS was significantly (p<0.05) effective in inhibiting hyperglycemia by 68%, decreased glycosylated haemoglobin by 20%, plasma and liver lipid profile except HDL-c and white blood cell count but increased the body weight by 17%, insulin, hepatic glycogen and red blood cell levels in comparison with diabetic untreated group. The results were comparable to glibenclamide (standard-drug). Histopathological studies on liver and pancreas of CAFS-treated rats showed regenerative effects.
 Conclusion: This study has indicated that CAFS possesses antihyperglycemic, antihyperlipidemic and ameliorative effect on diabetic induced abnormalities in haematological parameters, β-cell and liver tissue. The findings suggest that CAFS may be used as therapeutic adjunct in the management of diabetes.

Forkhead box O1 in turbot Scophthalmus maximus: Molecular characterization, gene structure, tissue distribution and the role in glucose metabolism

Forkhead box O1 (foxo1) is a transcription factor and plays important roles in glucose metabolism. In the present study, foxo1 in turbot Scophthalmus maximus was cloned and characterized. The siRNA of foxo1 was used to investigate the functions of foxo1 in turbot hepatocytes glucose metabolism. After that, a 10-week feeding trial with two different dietary carbohydrate levels (15% and 21%, respectively) was conducted to analyze the function of foxo1 in glucose metabolism in vivo. Results showed that the foxo1 was identified as 2176 bp (base pair) with a 2025 bp open reading frame, which encoded 675 amino acids. Sequence analysis showed that foxo1 of turbot was highly homologous to most of fishes. Tissue distribution analysis revealed that the highest expression of foxo1 was in liver. After in vitro analysis, foxo1-specific small interfering RNA (sifoxo1) treatment significantly decreased the expressions of cytosolic phosphoenolpyruvate carboxykinase (cpepck) and glucose-6-phosphatase1(g6pase1) in primary hepatocytes. Expression of mitochondrial phosphoenolpyruvate carboxykinase (mpepck) was not significantly inhibited. In contrast, the expression of glucose-6-phosphatase2 (g6pase2) increased significantly. After the in vivo study (feeding trial), with the decreased expression of foxo1 in turbot due to high dietary carbohydrate level (21%), the expression of g6pase2 was significantly upregulated. However, the expression of glucokinase (gk) was not changed significantly. These increased the level of blood glucose and hepatic glycogen. In conclusion, data from both in vitro (primary hepatocytes) and in vivo (feeding trial) showed that downregulated foxo1 in turbot could not result in significant depression of gluconeogenesis and activation of glycolysis. This could be one of the reasons why intake of high level of carbohydrate resulted in prolonged hyperglycemia in turbot.

Dietary supplementation with peanut skin polyphenolic extracts (PSPE) reduces hepatic lipid and glycogen stores in mice fed an atherogenic diet

Abstract The polyphenolic compounds found in red wine, grapes and peanut skins are bioactive compounds responsible for reduced mortality rates associated with cardiovascular disease. Resveratrol, a polyphenol found in the skin of grapes, reduced liver lipids and inflammation in mice fed an atherogenic diet. We aimed to assess the effects of polyphenolic compounds extracted from peanut skins by testing 3 treatments in mice (n = 10): atherogenic diet supplemented with peanut-skin polyphenolic extract (PSPE), atherogenic diet (ATH), and normal diet. Lymphocyte populations, blood glucose, hepatic cholesterol and glycogen and body weight (BW) were quantified at16 weeks. Mice fed the PSPE-diet had significantly improved BW, reduced hepatic glycogen and blood plasma glucose levels in comparison to the ATH treatment group. Moreover, hepatic cholesterol and lipid storage was reduced in mice fed the PSPE diet. Thus, PSPE could serve as a value added food and/or feed ingredient and an affordable plant source of antioxidants.

Evaluation of biochemical mechanisms of anti-diabetic functions of Anisomeles malabarica

Anisomeles malabarica (AM) is an aromatic plant traditionally used for the treatment of diabetes mellitus in India. Following bioassay guided fractionation, we recently identified an active fraction of AM (AMAF, with potential mix of active principles) that showed significant antihyperglycemic and antihyperlipidemic activities. In addition, AMAF treatment improved insulin levels. However, the biochemical mechanism/s through which AMAF demonstrates the antidiabetic effects is largely unknown. Based on its beneficial effects we investigated the biochemical mechanism of the anti-diabetic activity of A.malabarica active fraction (AMAF) in streptozotocin (STZ) induced diabetic rats. Streptozotocin induced diabetic rats were treated with AMAF (50 mg AMAF/kg/day) for 30 days and alterations in the body weights, glycogen and protein content of tissues, functional markers of hepatic and renal tissues, carbohydrate metabolic enzymes and their genes expression were evaluated. Lipid peroxides levels and activities of antioxidant enzymes of hepatic and renal tissues were also measured. The AMAF treatment resulted in increase in body weights, hepatic and renal protein and tissue glycogen levels in diabetic treated rats compared to diabetic rats. In addition, the treatment improved activities of carbohydrate metabolic enzymes, antioxidant enzymes and, liver and renal functional markers in the AMAF treated diabetic rats. Gene expressions of key carbohydrate metabolic enzymes/factors glucokinase, glucose transporter protein (GLUT-2) and phosphoenolpyruvate carboxykinase (PEPCK) were also normalized up on AMAF treatment in diabetic rats. Our studies indicate that the isolated active fraction of AM (AMAF) from the leaves of A.malabarica positively regulated the glucose homeostasis and oxidative stress through carbohydrate metabolism and antioxidant enzyme activities respectively in hepatic and renal tissues.

Evaluation of the effects of Ocimum basilicum essential oil in Nile tilapia diet: growth, biochemical, intestinal enzymes, haematology, lysozyme and antimicrobial challenges

Due to the intensification of tilapiculture, problems attributed to health of fish stocks have become more frequent. The objective of the present study was to evaluate growth, physiological responses and survival of Nile tilapia juveniles fed a diet containing the essential oil of Ocimum basilicum (EOOB) and infected by Aeromomas hydrophila. Five diets (in quadruplicates) were evaluated with increasing levels of EOOB (0.0 - control; 0.25; 0.5; 1.0 and 2.0 kg diet−1). On day 45, three fish from each tank were sampled and blood, intestine and liver samples were taken. On day 46, nine fish from each tank were infected with A. hydrophila followed by a 15-day period of observation. An addition of 2.0 mL EOOB in the diet improved the growth performance and increased haematological variables and activity of intestinal enzymes. Higher concentrations of EOOB in the diet reduced plasma triglycerides and glucose and hepatic glycogen and alanine aminotransferase (ALT) levels and increased plasma total proteins and ALT levels and lysozyme post-infection activity. The survival of fish after A. hydrophila infection was not influenced by the addition of EOOB in the diet. The use of 1.0 mL EOOB kg diet−1 seems to be more suitable than 2.0 mL EOOB kg diet−1 since the latter may be related to liver damage.

Biochanin A improves insulin sensitivity and controls hyperglycemia in type 2 diabetes

Biochanin A (5,7-Dihydroxy-4′-methoxyisoflavone) is an O-methylated isoflavone known for its anti-inflammatory, lipid lowering and anti-cancer activity. The current study was designed to find out antidiabetic efficacy of Biochanin A in type 2 diabetes in rats.Induction of type 2 diabetes mellitus in experimental animals was carried out by manipulation of diet using high fat diet for fourteen days and then administration of streptozotocin at low dose of 35 mg/kg, i.p. The diabetic animals were treated with 10, 20 and 40 mg/kg of Biochanin A for 28 days. The effect of Biochanin A treatment in diabetic animals was evaluated by measuring changes in body weight, biochemical parameters, insulin sensitivity index, Homeostatic model assessment-Insulin resistance (HOMA-IR), oral glucose tolerance test, glycohaemoglobin and hepatic glycogen level. Changes in histopathological characteristics of pancreatic tissue were also evaluated after treatment with Biochanin A. Immunohistochemical analysis of pancreatic tissue was carried out for the expression of SIRT1.The results showed that the selected doses of (10, 20 and 40 mg/kg) Biochanin A significantly decreased blood glucose (p < 0.001). The higher dose (40 mg/kg) of Biochanin A significantly reduced glucose tolerance (p < 0.001) in diabetic animals. Biochanin A treatment significantly reduced insulin resistance (p < 0.001) and improved inulin sensitivity (p < 0.01 for 10 mg/kg, 20 mg/kg, p < 0.001 for 40 mg/kg) at all selected dose levels. It also improved lipid profile significantly (p < 0.001) at lower, middle and higher dose level. Glycohaemoglobin formation was significantly decreased in diabetic animals (p < 0.001) after treatment with Biochanin A at all three dose levels. Liver glycogen level was also improved significantly after treatment with Biochanin A in diabetic animals at 20 mg/kg and 40 mg/kg dose level. Biochanin A at dose of 40 mg/kg increased SIRT1 expression in pancreatic tissue. In conclusion, Biochanin A has significant effect in type 2 diabetes mellitus which might be linked to its effects on SIRT1.

Formononetin Treatment in Type 2 Diabetic Rats Reduces Insulin Resistance and Hyperglycemia.

Type 2 diabetic mellitus is a multifactorial metabolic disorder affecting huge population around the world. This indicates that there is an urgent unmet need of cost effective, new treatment strategies for type 2 diabetes mellitus with no or less side effects. Phenolic compounds including isoflavones are known for their beneficial effect in metabolic disorders. The present work was intended to find out efficacy of formononetin, an isoflavone treatment in experimental model of type 2 diabetes. Type 2 diabetes mellitus was induced by feeding high fat diet for 2 weeks prior to streptozotocin administration in Sprague Dawley rats. Diabetic animals were treated with formononetin for 28 days at three dose level, i.e., 10, 20, and 40 mg/kg body weight orally. The effect of formononetin treatment on various parameters such as plasma glucose, glucose tolerance, insulin, HOMA-IR, lipid profile, hepatic glycogen content, glycohaemoglobin and SIRT1 expression in pancreatic tissue was measured. Histopathological changes in pancreatic tissue were also studied. Results of the study demonstrate that formononetin treatment reduces blood glucose level significantly (p < 0.001) at all the three dose level. It also improved glucose tolerance, insulin sensitivity and lipid profile along with reduction in glycohaemoglobin content in blood. Formononetin treatment also improved hepatic glycogen level profoundly in diabetic rats. Determination of SIRT1 expression in pancreatic tissue by immunohistochemical analysis showed that formononetin treatment increases the expression of SIRT1 in pancreatic tissue. Histopathological study showed that treatment with formononetin protects pancreatic beta cells from necro-degeneration and atrophic effect. It can be concluded that formononetin treatment reduces insulin resistance and attenuate hyperglycemia in type 2 diabetes which may be due to increasing expression of SIRT1 in pancreatic tissues.

Adaptation of Nile tilapia (Oreochromis niloticus) to different levels of dietary carbohydrates: New insights from a long term nutritional study

The objective of this study was to examine the long-term effects of different levels of dietary carbohydrates on glucose metabolism in the omnivorous Nile Tilapia (Oreochromis niloticus). Fish were fed from the first feeding stage until the adult stage, over a period of 40 weeks, using three different levels of carbohydrates (dextrin): 0% (CHO-L), 30% (CHO-M) and 50% (CHO-H). Growth performance, blood metabolite parameters, the proximate composition of the whole body, muscle and liver tissue, and the mRNA levels for genes involved in glycolysis, gluconeogenesis, lipogenesis and glucose transport in liver and muscle tissue were analyzed at week 26 and week 40. Fish fed the CHO-M diet exhibited the best growth performance, while the fish fed with the CHO-H diet showed the lowest growth performance. These data suggest that the incorporation of a certain level dietary carbohydrates can benefit Nile Tilapia. However, if the proportion of carbohydrates is very high, and concomitantly, the level of dietary proteins too low, this will not promote growth. Fish fed with carbohydrates exhibited a significant increase in lipid deposition in the whole body, muscle and liver tissues in. This seems to be due to increased lipogenic capacity, as reflected by higher hepatic fatty acid synthase mRNA levels and activity, as well as higher levels of plasma triglyceride. Nile Tilapia appear to be able to effectively adapt to the intake of carbohydrates, as reflected by: (i) the weak postprandial hyperglycemia (5.3–6.1 mM), (ii) the higher level of hepatic glycogen, (iii) the higher glycolytic pyruvate kinase enzyme in muscle (mRNA level and activity) and (iv) the inhibition of the gluconeogenic pathway for glucose-6-phosphatase and phosphoenolpyruvate carboxykinase enzymes (at molecular and enzymatic levels). Overall, these data show that the well-known differences in the capacity of carnivorous and omnivorous fish species to use dietary carbohydrates could be linked to differences in the regulation of the gluconeogenic and lipogenic pathways.

Relationship between genetic variation at PPP1R3B and levels of liver glycogen and triglyceride.

These observations are consistent with the notion that the minor allele of rs4841132 promotes a mild form of hepatic glycogenosis that is associated with hepatic injury. (Hepatology 2018;67:2182-2195).

Peripherally Administered Y2-Receptor Antagonist BIIE0246 Prevents Diet-Induced Obesity in Mice With Excess Neuropeptide Y, but Enhances Obesity in Control Mice.

Neuropeptide Y (NPY) plays an important role in the regulation of energy homeostasis in the level of central and sympathetic nervous systems (SNSs). Genetic silencing of peripheral Y2-receptors have anti-obesity effects, but it is not known whether pharmacological blocking of peripheral Y2-receptors would similarly benefit energy homeostasis. The effects of a peripherally administered Y2-receptor antagonist were studied in healthy and energy-rich conditions with or without excess NPY. Genetically obese mice overexpressing NPY in brain noradrenergic nerves and SNS (OE-NPYDβH) represented the situation of elevated NPY levels, while wildtype (WT) mice represented the normal NPY levels. Specific Y2-receptor antagonist, BIIE0246, was administered (1.3 mg/kg/day, i.p.) for 2 or 4.5 weeks to OE-NPYDβH and WT mice feeding on chow or Western diet. Treatment with Y2-receptor antagonist increased body weight gain in both genotypes on chow diet and caused metabolic disturbances (e.g., hyperinsulinemia and hypercholesterolemia), especially in WT mice. During energy surplus (i.e., on Western diet), blocking of Y2-receptors induced obesity in WT mice, whereas OE-NPYDβH mice showed reduced fat mass gain, hepatic glycogen and serum cholesterol levels relative to body adiposity. Thus, it can be concluded that with normal NPY levels, peripheral Y2-receptor antagonist has no potential for treating obesity, but oppositely may even induce metabolic disorders. However, when energy-rich diet is combined with elevated NPY levels, e.g., stress combined with an unhealthy diet, Y2-receptor antagonism has beneficial effects on metabolic status.

Influence of vegetable diets on physiological and immune responses to thermal stress in Senegalese sole (Solea senegalensis).

The substitution of fish resources as ingredients for aquafeeds by those based on vegetable sources is needed to ensure aquaculture sustainability in the future. It is known that Senegalese sole (Solea senegalensis) accepts high dietary content of plant ingredients without altering growth or flesh quality parameters. However, scarce information is available regarding the long-term impact of vegetable diets (combining the inclusion of both vegetable protein and oils) on the stress response and immunity of this fish species. This study aims to evaluate the concomitant effect of the extended use of vegetable protein-based diets with fish oil (FO) replacement (0, 50 or 100%) by vegetable oils (VO), on the response to acute (10 min) or prolonged (4 days) stress, induced by thermal shock. Plasma levels of cortisol, glucose and lactate as well as hepatic levels of glucose, glycogen and lactate were evaluated as primary and secondary responses to stress, 6 and 18 months after feeding the experimental diets (6 and 18 MAF). The brain monoaminergic activity in telencephalon and hypothalamus, and non-specific immune parameters were also evaluated. As expected, thermal shock induced an increase in values of plasma parameters related to stress, which was more evident in acute than in prolonged stress. Stress also affected lactate levels in the liver and the values of the alternative complement pathway-ACH50 in the plasma. Dietary substitution of FO induced an effect per se on some parameters such as decreased hepatic glucose and glycogen levels and peroxidase activity in plasma as well enhanced serotonergic activity in brain of non-stressed fish. The results obtained in some parameters indicate that there is an interaction between the use of vegetable diets with the physiological response to thermal stress, as is the case of the hepatic lactate, serotonergic neurotransmission in brain, and the activity of ACH50 in plasma. These results suggest that the inclusion of VO in plant protein based diets point to a slightly inhibited stress response, more evident for an acute than a prolonged stress.

Acute and sublethal effects of organophosphate insecticide chlorpyrifos on freshwater fish Oreochromis niloticus

Chlorpyrifos is a widely used organosphosphate insecticide in India. Residue of the insecticide is frequently detected in trace to moderate concentration in food grains and in surface water of different freshwater ecosystems of the country. In this study, 96 h LC50 of the technical grade (94% a.i.) and commercial formulation (20% EC) of chlorpyrifos to freshwater fish Oreochromis niloticus were determined as 90.0 and 42.0 µg/L based on 2 h actual concentration of chlorpyrifos in water. About 96 h exposure to sublethal concentrations (0, 12.0 and 25.0 μg/L) of the commercial formulation (20% EC) of chlorpyrifos reduced the level of hepatic glycogen, activities of alkaline phosphatase, acetylcholinesterase, and catalase in liver and elevated the level of plasma glucose and activities of hepatic acid phosphatase, aspartate aminotransferase, and alanine aminotransferase in O. niloticus. About 28-day exposure to these sub-lethal concentrations caused anemia in fish, while 90 days exposure reduced growth of the fish and carcass concentration of crude protein and crude lipid as compared to control. It was concluded from this study that commercial formulation of chlorpyrifos (20% EC) was highly toxic to O. niloticus. Exposure to sub-lethal concentrations of the insecticide could induce oxidative stress and anemia resulting in reduced growth of the fish.

The Antidiabetic and Antinephritic Activities of Tuber melanosporum via Modulation of Nrf2‐Mediated Oxidative Stress in the db/db Mouse

Tuber melanosporum (TM), a valuable edible fungus, contains 19 types of fatty acid, 17 types of amino acid, 6 vitamins, and 7 minerals. The antidiabetic and antinephritic effects of TM and the underlying mechanisms related to oxidative stress were investigated in db/db mice. Eight-week oral administration of metformin (Met) at 0.1 g/kg and TM at doses of 0.2 and 0.4 g/kg decreased body weight, plasma glucose, serum levels of glycated hemoglobin, triglyceride, and total cholesterol and increased serum levels of high-density lipoprotein cholesterol in the mice, suggesting hypoglycemic and hypolipidemic effects. TM promoted glucose metabolism by increasing the levels of pyruvate kinase and hepatic glycogen. It also regulated the levels of inflammatory factors and oxidative enzymes in serum and/or the kidneys of the mice. Additionally, TM increased the expression of nuclear respiratory factor 2 (Nrf2), catalase, heme oxygenase 1, heme oxygenase 2, and manganese superoxide dismutase 2 and decreased the expression of protein kinase C alpha, phosphor-janus kinase 2, phosphor-signal transducer and activator of transcription 3, and phosphor-nuclear factor-κB in the kidneys. The results of this study reveal the antidiabetic and antidiabetic nephritic properties of TM via modulating oxidative stress and inflammation-related cytokines through improving the Nrf2 signaling pathway.

Carbohydrate tolerance in the fruit-eating fish Piaractus mesopotamicus (Holmberg, 1887)

Some fish species have a limited ability to metabolize dietary carbohydrates. An important tool for understanding carbohydrate metabolism is the application of the glucose tolerance test, which can be performed orally or intraperitoneally. To evaluate carbohydrate tolerance in the fruit-eating fish pacu, two experiments were performed, one with oral administration by gavage of three carbohydrate types (glucose, fructose and starch, 2.0 g/kg body weight (BW)) and the other with intraperitoneal injection (IP) of glucose (500 mg/kg BW). Oral glucose resulted in an increase in plasma glucose 2 hr later with the peak at 4 hr (8.30 mmol/L), and return to baseline between 6 and 12 hr; starch administration promoted a peak after 4 hr (7.70 mmol/L), returning to the baseline at 6 hr. The administration of fructose promoted a moderate peak after 2 hr (5.71 mmol/L), and return to baseline for the time points that followed. Elevated serum cholesterol levels were observed 2 and 24 hr after administration of glucose and starch. Hepatic glycogen levels increased within 24 hr, regardless of the type of carbohydrate administered. IP glucose load resulted in a peak of plasma glucose 3 hr post injection (6.91 mmol/L), returning to baseline 6 hr later. There was a reduction in the concentration of triglycerides at 24 hr. The results demonstrate that pacu metabolize both oral (glucose or starch) and intraperitoneal (glucose) carbohydrate loads after 6 hr, suggesting good ability to deal with dietary carbohydrates.

Hepatic glycogen levels in female rats submitted to aquatic therapy after muscle disuse

The aim of the present study was to analyse the changes in liver glycogen content in rats subjected to aquatic therapy post-disuse of the paw. 32 wistar adult female rats were equally divided: Control (C), kept in the cage for two weeks without interventions; Disuse (D) had the right paw immobilized with hip extension, knee and plantar flexion for two weeks; Aquatic Therapy (AT) underwent aquatic therapy with increments of 3 minutes daily for two weeks, totalizing 36 minutes of training; Disused Aquatic Therapy (DTA) was first subjected to immobilization for two weeks and 24 hours after withdrawal of immobilization aquatic therapy was started for two more weeks, in same protocols of D and AT groups. At the end of the experiment, the animals were sacrificed, and tissues were dissected, weighed and stored. The liver tissues were referred analysis of glycogen content. It was observed that the blood glucose levels of the AT group (104 mg/dL) were different from the C group (86 mg/dL; p = 0.0213). Regarding hepatic glycogen, the D (2.35mg±0.07) and AT (2.73mg±0.07) groups had hepatic glycogen reduction by 22% and 15%, relative to C (2.51mg±0.03); p &lt;0.0001). The DTA group presented no differences when compared to the control, suggesting the normalization of the finding. Muscle disuse by two weeks promoted changes in glycogen levels, however, two weeks after disuse condition, the aquatic therapy were able to correct the energetic reserve in liver.

PRMT1 promotes hyperglycemia in a FoxO1-dependent manner, affecting glucose metabolism, during hypobaric hypoxia exposure, in rat model.

High-altitude (HA) environment causes changes in cellular metabolism among unacclimatized humans. Previous studies have revealed that insulin-dependent activation of protein kinase B (Akt) regulates metabolic processes via discrete transcriptional effectors. Moreover, protein arginine methyltransferase (PRMT)1-dependent arginine modification of forkhead box other (FoxO)1 protein interferes with Akt-dependent phosphorylation. The present study was undertaken to test the involvement of PRMT1 on FoxO1 activation during hypobaric hypoxia (HH) exposure in rat model. Samples were obtained from normoxia control (NC) and HH-exposed (H) rats, subdivided according to the duration of HH exposure. To explore the specific role played by PRMT1 during HH exposure, samples from 1d pair-fed (PF) NC, 1d acute hypoxia-exposed (AH) placebo-treated, and 1d AH TC-E-5003-treated rats were investigated. Quantitative reverse transcriptase polymerase chain reaction (RT-qPCR) was performed to determine expressions of glycolytic, gluconeogenic enzymes, and insulin response regulating genes. Immuno-blot and enzyme linked immunosorbent assay (ELISA) were used for insulin response regulating proteins. Nuclear translocation of FoxO1 was analyzed using deoxyribonucleic acid (DNA)-binding ELISA kit. We observed HH-induced increase in glycolytic enzyme expressions in hepatic tissue unlike hypothalamic tissue. PRMT1 expression increased during HH exposure, causing insulin resistance and resulting increase in FoxO1 nuclear translocation, leading to hyperglycemia. Conversely, PRMT1 inhibitor treatment promoted inhibition of FoxO1 activity and increase in glucose uptake during HH exposure leading to reduction in blood-glucose and hepatic glycogen levels. PRMT1 might have a potential importance as a therapeutic target for the treatment of HH-induced maladies.

Anti-diabetic effects of Inonotus obliquus polysaccharides in streptozotocin-induced type 2 diabetic mice and potential mechanism via PI3K-Akt signal pathway

Polysaccharides are the main components of mushroom Inonotus obliquus (I. obliquus) with antihyperglycemic activities. This study was aimed to investigate the anti-diabetic effects and the potential mechanism of I. obliquus polysaccharides (IOPS) in high fat diet and STZ-induced type 2 diabetic mice. Results showed that oral administration of IOPS (900mg/kg) could significantly restore the body and fat mass weight, reduce fasting blood glucose levels, improve glucose tolerance ability, increase hepatic glycogen level and ameliorate insulin resistance compared to those of the control diabetic mice (P<0.01). IOPS (900mg/kg) could enhance the cholesterol transportation in the liver, which was in coincidence with the increased HDL-C levels and decreased TC, TG and LDL-C levels.Treatment of IOPS could significantly improve the antioxidant activities of liver (P<0.05) and alleviate the STZ-lesioned organ tissues (liver, kidney, and pancreas). Further, protein expressions of PI3K-p85, p-Akt (ser473), GLUT4 were up-regulated after IOPS treatment, indicating that the antihyperglycemic mechanism of IOPS might involve in activating PI3K and Akt phosphorylation as well as the translocation of GLUT4 in diabetic mice. The results suggested that IOPS might be a promising functional food or drug candidate for diabetes treatment.