Blood Glucose In Diabetic Mice Research Articles

Pinctada martensii Hydrolysate Modulates the Brain Neuropeptidome and Proteome in Diabetic (db/db) Mice via the Gut-Brain Axis.

Pinctada martensii hydrolysate (PMH) has been proved to have the effect of ameliorating disorders of glucose and lipid metabolism in db/db mice, but the mechanism of its hyperglycemia effect is still unclear. Bacterial communities in fecal samples from a normal control group, a diabetic control group, and a PMH-treated diabetes mellitus type 2 (T2DM) group were analyzed by 16S gene sequencing. Nano LC-MS/MS was used to analyze mice neuropeptides and proteomes. The 16S rDNA sequencing results showed that PMH modulated the structure and composition of the gut microbiota and improved the structure and composition of Firmicutes and Bacteroidetes at the phylum level and Desulfovibrionaceae and Erysipelatoclostridiaceae at the family level. Furthermore, the expressions of functional proteins of the central nervous system, immune response-related protein, and proteins related to fatty acid oxidation in the brain disrupted by an abnormal diet were recovered by PMH. PMH regulates the brain neuropeptidome and proteome and further regulates blood glucose in diabetic mice through the gut-brain axis. PMH may be used as a prebiotic agent to attenuate T2DM, and target-specific microbial species may have unique therapeutic promise for metabolic diseases.

4S-fluorination of ProB29 in insulin lispro slows fibril formation

Recombinant insulin is a life-saving therapeutic for millions of patients affected by diabetes mellitus. Standard mutagenesis has led to insulin variants with improved control of blood glucose; for instance, the fast-acting insulin lispro contains two point mutations that suppress dimer formation and expedite absorption. However, insulins undergo irreversible denaturation, a process accelerated for the insulin monomer. Here we replace ProB29 of insulin lispro with 4R-fluoroproline, 4S-fluoroproline, and 4,4-difluoroproline. All three fluorinated lispro variants reduce blood glucose in diabetic mice, exhibit similar secondary structure as measured by circular dichroism, and rapidly dissociate from the zinc- and resorcinol-bound hexamer upon dilution. Notably, however, we find that 4S-fluorination of ProB29 delays the formation of undesired insulin fibrils that can accumulate at the injection site in vivo, and can complicate insulin production and storage. These results demonstrate how subtle molecular changes achieved through non-canonical amino acid mutagenesis can improve the stability of protein therapeutics.

Nephroprotective effect of HZF by upregulating IκBα protein expression in DKD mice

HEZHIFNAG (HZF) is a traditional Chinese prescription used to treat diabetes. In this study, a mouse model of diabetic kidney disease (DKD) induced by alloxan was used, and the random blood glucose of diabetic mice decreased significantly after the intervention of HZF, and the morphological results showed that HZF improved the pathological damage of glomeruli, reduced the degree of fibrosis of kidney tissue, and increased the expression level of IKBα in the kidney of diabetic mice, suggesting that HZF has a protective effect on the DKD mice, and the mechanism of action may be related to the up-regulation of IKB-α expression.

The effect of Astragalus polysaccharide nanoparticles on blood glucose in diabetic mice

The effect of Astragalus polysaccharide nanoparticles on blood glucose in diabetic mice

Carboxymethyl chitosan-TK resistant starch complex ameliorates type 2 diabetes by regulating the gut microbiota

Carboxymethyl chitosan and resistant starch exhibit good performance in diabetes regulation. We prepared carboxymethyl chitosan - resistant starch complex. Test the properties of composite resistant starch by using X-ray diffraction, water contact angle, infrared spectroscopy, and scanning electron microscopy, interactions with intestinal microbiota and mouse experiments were also conducted. The results indicated that the composite resistant starch had a good effect on promoting the proliferation of probiotics on Bifidobacterium and a significant inhibitory effect on Escherichia coli than resistant starch (P < 0.05). After administration, the water intake and weight of diabetic mice were significantly reduced. The blood glucose of diabetic mice was also reduced, and oral glucose tolerance showed that the glucose degradation rates of composite resistant starch were significantly improved compared to model mice. Cholesterol, triglycerides, high-density lipoprotein and low-density lipoprotein were significantly lower than those in the diabetes group (P < 0.05). The diversity of the gut microbiota was also proven.

Study on the therapeutic effect and mechanism of Tangningtongluo Tablet on diabetic mice

AimsTo investigate the therapeutic effects of Tangningtongluo Tablet on diabetic mice and its mechanism. This study was established the scientific basis for the clinical application of Tangningtongluo Tablet in the treatment of diabetes mellitus and provided data supporting the transformation of Tangningtongluo Tablet from an in-hospital preparation to a new Chinese medicine. MethodsIn this study, a diabetic mouse model was established by high-glucose and high-fat diet feeding in combination with STZ injection for 4 weeks. Glucose metabolism, lipid metabolism, liver histomorphological changes and liver function related indexes were detected, pancreatic histomorphological changes and insulin resistance related indexes were observed, and the expression of pathway related proteins and inflammatory factors were examined. ResultsGlycemia and glycated hemoglobin were reduced in diabetic mice after the treatment of Tangningtongluo Tablet, and glucose tolerance and lipid results were modified. The insulin resistance status of the mice was diminished and tissue damage to the pancreas and liver was repaired. Expression of ERS/NF-κB related pathway proteins was reduced in liver tissues, and inflammatory factors such as TNF-α, IL-6 and IL-1β were reduced in serum. ConclusionsTangningtongluo Tablet could reduce blood glucose in diabetic mice, regulate the disorder of lipid metabolism, enhance insulin sensitivity, improve insulin resistance, repair pancreatic tissue damage and protect mouse liver in diabetic mice. The mechanism of action might be related to the regulation of ERS/NF-κB signaling pathway and the reduction of TNF-α, IL-6 and IL-1β production.

Astragalin ameliorates renal injury in diabetic mice by modulating mitochondrial quality control via AMPK-dependent PGC1α pathway.

Diabetic kidney disease (DKD) is a common microvascular complication of diabetes mellitus, and oxidative stress and mitochondrial dysfunction play an important role in this process. It has been shown that aldose reductase (ALR2) catalyzes NADPH-dependent reduction of glucose to sorbitol, resulting in oxidative stress and mitochondrial dysfunction in diabetic patients. Astragalin (AG), a flavonoid extracted from Thesium chinense Turcz., shows an inhibitory activity on ALR2. In this study, we investigated the therapeutic effects of AG against renal injury in streptozocin (STZ)-induced diabetic mouse model. Diabetic mice were orally administered AG (5, 10 mg·kg-1·d-1) for 4 weeks. We showed that AG treatment greatly improved the proteinuria and ameliorated renal pathological damage without affecting the elevated blood glucose in diabetic mice. Furthermore, AG treatment significantly suppressed highly activated ALR2, and reduced oxidative stress in the kidney of diabetic mice and in high glucose and lipids-stimulated HK2 cells in vitro. We demonstrated that AG treatment modulated mitochondrial quality control and ameliorated apoptosis, boosting mitochondrial biogenesis, maintaining mitochondrial dynamic homeostasis, and improving energy metabolism disorder in vivo and in vitro. In high glucose and lipids-stimulated HK2 cells, we found that AG (20 μM) restored the phosphorylation level of AMPK, and upregulated the expression and transcriptional activity of PGC1α, whereas treatment with H2O2, blockade of AMPK with Compound C or knockdown of AMPKα with siRNA abolished the protective effect of AG on mitochondrial function, suggesting that antioxidant effects and activation of AMPK-dependent PGC1α pathway might be the molecular mechanisms underlying the protective effects of AG on mitochondrial quality control. We conclude that AG could be a promising drug candidate for the treatment of diabetic renal injury through activating AMPK.

TRIM62 knockdown by inhibiting the TLR4/NF-κB pathway and NLRP3 inflammasome attenuates cognitive impairment induced by diabetes in mice.

The tripartite motif 62 is an E3 ubiquitin ligase protein that regulates cellular processes, including differentiation, immunity, development and apoptosis, leading to various disease states, such as cancer and inflammatory diseases. However, the role and mechanism of the tripartite motif 62 in the process of diabetic-induced cognitive impairment have not been reported. Therefore, the aim of this study was to investigate the role and mechanism of the tripartite motif 62 in diabetic-induced cognitive impairment. The results showed that the expression of the tripartite motif 62 was up-regulated in diabetic mice. Silencing of TRIM62 increased body weight and decreased fasting blood glucose in diabetic mice. In addition, knockdown of the tripartite motif 62 inhibited STZ-induced inflammation, apoptosis and oxidative stress. Further studies showed that the TLR4/NF-κB pathway and NLRP3 inflammasomes were involved in the regulation of diabetic mice by the tripartite motif 62. More importantly, inhibition of the tripartite motif 62 improved cognitive impairment and learning ability in mice. In conclusion, inhibition of TRIM62 inhibits STZ-induced inflammation, cell apoptosis and oxidative stress, and improves the cognitive ability of mice. Therefore, the tripartite motif 62 may be an important target for the treatment of diabetes-induced cognitive impairment.

DAMP-modulating nanoparticle for successful pancreatic islet and stem cell transplantation

Cell therapy is targeted at many organs, but locally or systemically delivered cells are shortly able to survive resulting from the immune/inflammation reactions and irregular cell targeting. Here we explore the multimodal nanoparticle having anti-inflammation and magnetic guidance for successful cell transplantation. We design magnetic resonance (MR)-active glycyrrhizin-chitosan coated superparamagnetic iron oxide nanoparticle (SPIO@Chitosan-GL) to inhibit release of inflammatory damage-associated molecular pattern (DAMP) protein and to offer noninvasive monitoring after intrahepatic transplantation of pancreatic islets and mesenchymal stem cell (MSC) spheroids. Intracellular delivered SPIO@Chitosan-GL is not cytotoxic to pancreatic islets and MSC spheroids and attenuate DAMP release from them. Also, therapeutic cells labeled with SPIO@Chitosan-GL are magnetically localized to the intended lobe of liver during transplantation procedure. If necessary, partial hepatectomy can be performed to remove the localized therapeutic cells for protection of the remaining liver lobes from systemic inflammation. Therapeutically, the cells selectively localized in the liver can treat blood glucose in diabetic mice to normal levels with DAMP modulation, and are visualized using in vivo MR imaging for over 4 weeks. Collectively, DAMP-modulating SPIO@Chitosan-GL can be used in multimodal nanomedince for attenuating the inflammation reaction by transplanted cells and for noninvasively long-term monitoring of transplanted cells.

Cardioprotective Effects of 1-(3,6-Dibromo-carbazol-9-yl)-3-Phenylamino-Propan-2-Ol in Diabetic Hearts via Nicotinamide Phosphoribosyltransferase Activation.

Diabetes is associated with increased cardiac injury and sudden death. Nicotinamide phosphoribosyltransferase (Nampt) is an essential enzyme for the NAD+ salvage pathway and is dysregulated in diabetes. Nampt activation results in rescued NADH/NAD+ ratios and provides pharmacological changes necessary for diabetic cardioprotection. Computer docking shows that 1-(3,6-Dibromo-carbazol-9-yl)-3-phenylamino-propan-2-ol (P7C3) allows for enhanced Nampt dimerization and association. To test the pharmacological application, we used male leptin receptor-deficient (db/db) mice and treated them with Nampt activator P7C3. The effects of 4-week P7C3 treatment on cardiac function were evaluated along with molecular signaling changes for phosphorylated protein kinase B (p-AKT), phosphorylated endothelial nitric oxide synthase (p-eNOS), and sirtuin 1 (SIRT1). The cardiac function evaluated by ECG and echocardiography were significantly improved after 4 weeks of P7C3 treatment. Biochemically, higher NADH/NAD+ ratios in diabetic hearts were rescued by P7C3 treatment. Moreover, activities of Nampt and SIRT1 were significantly increased in P7C3-treated diabetic hearts. P7C3 treatment significantly decreased the blood glucose in diabetic mice with 4-week treatment as noted by glucose tolerance test and fasting blood glucose measurements compared with vehicle-treated mice. P7C3 activated Nampt enzymatic activity both in vitro and in the 4-week diabetic mouse hearts, demonstrating the specificity of the small molecule. P7C3 treatment significantly enhanced the expression of cardioprotective signaling of p-AKT, p-eNOS, and Beclin 1 in diabetic hearts. Nampt activator P7C3 allows for decreased infarct size with decreased Troponin I and lactose dehydrogenase (LDH) release, which is beneficial to the heart. Overall, the present study shows that P7C3 activates Nampt and SIRT1 activity and decreases NADH/NAD+ ratio, resulting in improved biochemical signaling providing cardioprotection. SIGNIFICANCE STATEMENT: This study shows that 1-(3,6-Dibromo-carbazol-9-yl)-3-phenylamino-propan-2-ol (P7C3) is effective in treating diabetes and cardiovascular diseases. The novel small molecule is antiarrhythmic and improves the ejection fraction in diabetic hearts. The study successfully demonstrated that P7C3 decreases the infarct size in hearts during myocardial infarction and ischemia-reperfusion injury. Biochemical and cellular signaling show increased NAD+ levels, along with Nampt activity involved in upregulating protective signaling in the diabetic heart. P7C3 has high therapeutic potential for rescuing heart disease.

Korean naked waxy barley (saechalssal) extract reduces blood glucose in diabetic mice by modulating the PI3K-Akt-GSK3β pathway.

Saechalssal barley is Korea's representative naked waxy barley. This study investigated the anti-diabetic effect of the extract derived from saechalssal and its mechanism. The prethanol extract of saechalssal (SPE) showed greater α-glucosidase inhibitory activity in vitro and a more significant lowering of the postprandial blood glucose levels in normal mice compared to its water extract (SWE). When mice with type 2 diabetes (T2DM) induced by a high-fat diet and streptozotocin were fed SPE (200mg/kg/day) for six weeks, the fasting blood glucose and serum free fatty acid levels were significantly lower than those of the control group. SPE significantly elevated the hepatic glycogen accumulation with increasing glycogen synthesis-related gene (GYS2 and UGP2) levels compared to the control group. SPE stimulated the expression of the hepatic glycolysis-related genes (GK, PFK1, and PK) and suppressed the gluconeogenesis-related genes (G6Pase, FBP1, and PEPCK). SPE up-regulated the phosphorylation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt), whereas it down-regulated the phosphorylation of glycogen synthase kinase 3 beta (GSK3β) compared to the control. The major flavonoids of SPE were naringin, prunin, and catechin, while its phenolic acids were ferulic acid and vanillic acid. These phytochemical compounds may contribute to the anti-hyperglycemic effects of SPE in diabetes. Overall, these results suggest that SPE has potential anti-diabetic activity through the regulating the PI3K/Akt/GSK3β pathway.

Blocking Kir6.2 channels with SpTx1 potentiates glucose-stimulated insulin secretion from murine pancreatic β cells and lowers blood glucose in diabetic mice.

ATP-sensitive K+ (KATP) channels in pancreatic β cells are comprised of pore-forming subunits (Kir6.2) and modulatory sulfonylurea receptor subunits (SUR1). The ATP sensitivity of these channels enables them to couple metabolic state to insulin secretion in β cells. Antidiabetic sulfonylureas such as glibenclamide target SUR1 and indirectly suppress Kir6.2 activity. Glibenclamide acts as both a primary and a secondary secretagogue to trigger insulin secretion and potentiate glucose-stimulated insulin secretion, respectively. We tested whether blocking Kir6.2 itself causes the same effects as glibenclamide, and found that the Kir6.2 pore-blocking venom toxin SpTx1 acts as a strong secondary, but not a strong primary, secretagogue. SpTx1 triggered a transient rise of plasma insulin and lowered the elevated blood glucose of diabetic mice overexpressing Kir6.2 but did not affect those of nondiabetic mice. This proof-of-concept study suggests that blocking Kir6.2 may serve as an effective treatment for diabetes and other diseases stemming from KATP hyperactivity that cannot be adequately suppressed with sulfonylureas.

Hypoglycemic effect of leaf extract of Pseuderanthemum crenulatum leaves in an alloxan-induced diabetic mice

In this study, the hypoglycaemic effects of ethanol extracts from Pseuderanthemum crenulatum leaves were investigated. The evaluated trials included: in vitroα-glucosidase inhibitory activity; oral glucose tolerance test in normoglycemic mice; hypoglycemia in an alloxan-induced diabetic mice model, and oral toxicity assay. The results showed that the ethanol extract of P. crenulatumleaves was able to inhibit α-glucosidase enzyme at IC50=66.01 μg/ml, 1.8 times higher than acarbose control (IC50 was 122.2 μg/ml). After 21 days of using leaf extract of P. crenulatum (1 g/kg) to treat diabetic mice, the blood glucose was reduced by 42.02%. This result was equivalent to gliclazide (10 mg/kg) which reduced the blood glucose of diabetic mice by 41.78%. The oral toxicity test results at a dose of 5 g/kg equivalent to 357 g of fresh leaf/kg after 72 hours was not exhibited acute oral toxicity in mice. In summary, there is a need for more studies on the ability of P. crenulatum leaves to treat diabetes.

Maslinic acid activates renal AMPK/SIRT1 signaling pathway and protects against diabetic nephropathy in mice

BackgroundDiabetic nephropathy has been a devastating complication. Clinically, there is an urgent need for nephroprotective agents to delay the onset of diabetic nephropathy and ameliorate its symptoms. Maslinic acid is a pentacyclic triterpene acid with protective effect on multiple organs against oxidative stress and inflammation. In this research, we hypothesized that maslinic acid protects renal function against diabetic nephropathy.MethodsC57BL/6 J male mice administrated with 50 mg/kg of Streptozocin (STZ) daily were used to establish diabetic mouse model (blood glucose levels > 300 mg/dL). Urinary levels of albumin, total proteins, and creatinine were analyzed by an automatic analyzer. H&E staining was used to evaluate renal damage. qRT-PCR and ELISA were performed to investigate the inflammation and oxidative stress in renal tissues. Western blot was used to assess the activation of AMPK signaling.ResultsMaslinic acid treatment alleviated the loss of body weight and blood glucose in diabetic mice. Renal structure and function were protected by maslinic acid in diabetic mice. 20 mg/kg maslinic acid treatment for 8 weeks significantly alleviated the oxidative stress and inflammation in the kidney of diabetic rats. Maslinic acid treatment activated the renal AMPK/SIRT1 signaling pathway.ConclusionMaslinic acid ameliorates diabetic nephropathy and activates the renal AMPK/SIRT1 signaling pathway.

Effects of sweet corncob polysaccharide on pancreatic protein expression in type 2 diabetic rats

The cobs of sweet corn, also known as vegetable corn, are a nutritionally rich agricultural by-product. Sweet corncob polysaccharide (SCP-80-I) is a bioactive macromolecule extracted from the sweet corncob. Previous studies have shown that SCP-80-I has beneficial biological activities, including anti-oxidative and hypoglycemic properties. Previously, we showed that SCP-80-I had hypoglycemic effects, but the overall molecular changes associated with SCP-80-I have not yet been clarified in vivo. In this study, we investigated the hypoglycemic effects of SCP-80-I in diabetic rats with insulin resistance and analyzed the hypoglycemic mechanisms of SCP-80-I using tandem mass tag (TMT) -labeled quantitative proteomics. Using gene onotology (GO) annotations and kyoto encyclopedia of genes and genomes (KEGG) pathway analysis, the biological process, cell composition, and molecular function terms associated with the differentially expressed proteins were identified, as were the associated signaling pathways. In total, 4780 proteins exhibited a fold-change greater than 1.5. Six differentially expressed proteins related to the development and treatment of diabetes were selected, encoded by the genes Pik3r5, Ndufb3, Pygl, Cbl, Prkcd, and Stat1. SCP-80-I induced hypoglycemia mainly through the PI3K-Akt and JAK-STAT signaling pathways. SCP-80-I also ameliorated diabetes by regulating the expression of the Pik3r5, Ndufb3, Pygl, Cbl, Prkcd, and Stat1 genes. This study provided a theoretical basis for the treatment of diabetes and the development of hypoglycemic drugs. Our results suggested that SCP-80-I plays a beneficial role in reducing blood glucose in diabetic mice, which helps to clarify the molecular mechanisms by which sweet corncob polysaccharide reduces blood glucose.

A polysaccharide isolated from Ganoderma lucidum ameliorates hyperglycemia through modulating gut microbiota in type 2 diabetic mice

In this study, we reported a thermal stable and non-toxic heteropolysaccharide F31, which decreased the blood glucose of diabetic mice (21.75 mmol/L) induced by high-fat diet (HFD) and streptozotocin (STZ) to 12.56 and 15.18 mmol/L (P < 0.01) at 180 and 60 mg/kg, depicting remarkable hypoglycemic effects of 42.25 and 30.21%. Moreover, F31 repaired islet cells and increased insulin secretion, promoted the synthesis and storage of glycogen in liver and improved activities of antioxidant enzymes and insulin resistances, declining HOMA-IR (43.77 mmol/mU) of diabetic mice (P < 0.01) to 17.32 and 20.96 mmol/mU at both doses. 16S rRNA gene sequencing revealed that F31 significantly decreased Firmicutes (44.92%, P < 0.01) and enhanced Bacteroidetes (33.73%, P < 0.01) and then increased B/F ratio of diabetic mice to 0.6969 (P < 0.01), even being close to normal control (P = 0.9579). F31 enriched Lactobacillus, Bacteroides and Ruminococcaceae, which may relieve glucose, insulin resistance and inflammation through decreasing the release of endotoxins into the circulation from intestine, carbohydrate fermentation in gut and activation of the intestine-brain axis. Functionally, F31 improved metabolism of gut microbiota to a normal state. These results may provide novel insights into the beneficial effect of F31 against hyperglycemia.

Effect of mulberry galacto-oligosaccharide isolated from mulberry on glucose metabolism and gut microbiota in a type 2 diabetic mice

• Mulberry galacto-oligosaccharide (MGO) could reduce blood sugar fluctuations in type 2 diabetic mice. • MGO alleviates the oxidative stress. • MGO up-regulates PI3K/Akt pathways in type 2 diabetic mice. • MGO displayed a positive effect in the liver glucose metabolism pathways. • MGO was able to change the fecal microbiota in type 2 diabetic mice. Mulberry possesses many biological characteristics, such as reduce blood sugar and antioxidant properties, but whether mulberry galacto-oligosaccharide (MGO) can impact the characteristics of the gut microbiota is not yet clear. The objective of this work was to investigate the protective effects of MGO in type 2 diabetic (T2D) mice. The analysis of typical diabetic symptoms and serum status showed that oral MGO alleviated hyperglycemia, insulin resistance and oxidative stress in diabetic mice. These changes were caused by up-regulating the expression of key proteins in the PI3K/Akt pathway, involved in the control of liver glycolysis and gluconeogenesis, and liver glucose metabolism having a positive hypoglycemic effect. Additionally, the gut microbiota indicated that MGO treatment could positively modulate the microbiome composition to decrease the blood glucose in diabetic mice by promoting the growth of Prevotellaceae and Lactobacillus, whereas decreasing the abundance of Lachnospiraceae .

Mangosteen xanthone γ-mangostin exerts lowering blood glucose effect with potentiating insulin sensitivity through the mediation of AMPK/PPARγ

Diabetes mellitus (DM) is concomitant with significant morbidity and mortality and its prevalence is accumulative in worldwide. The conventional antidiabetic agents are known to mitigate the symptoms of diabetes; however, they may also cause side and adverse effects. There is an imperative necessity to conduct preclinical and clinical trials for the discovery of alternative therapeutic agents that can overcome the drawbacks of current synthetic antidiabetic drugs. This study aimed to investigate the efficacy of lowering blood glucose and underlined mechanism of γ-mangostin, mangosteen (Garcinia mangostana) xanthones. The results showed γ-Mangostin had a antihyperglycemic ability in short (2 h)- and long-term (28 days) administrations to diet-induced diabetic mice. The long-term administration of γ-mangostin attenuated fasting blood glucose of diabetic mice and exhibited no hepatotoxicity and nephrotoxicity. Moreover, AMPK, PPARγ, α-amylase, and α-glucosidase were found to be the potential targets for simulating binds with γ-mangostin after molecular docking. To validate the docking results, the inhibitory potency of γ-mangostin againstα-amylase/α-glucosidase was higher than Acarbose via enzymatic assay. Interestingly, an allosteric relationship between γ-mangostin and insulin was also found in the glucose uptake of VSMC, FL83B, C2C12, and 3T3-L1 cells. Taken together, the results showed that γ-mangostin exerts anti-hyperglycemic activity through promoting glucose uptake and reducing saccharide digestion by inhibition of α-amylase/α-glucosidase with insulin sensitization, suggesting that γ-mangostin could be a new clue for drug discovery and development to treat diabetes.

Antidiabetic activity of galactomannan from Chinese Sesbania cannabina and its correlation of regulating intestinal microbiota

The purpose of this study was to evaluate the antidiabetic activity of galactomannan (SP) extracted from endosperm splits of Chinese Sesbania cannabina seeds based on the animal experiments and discuss the effects of SP on the regulation of intestinal microbiota in streptozotocin (STZ) induced diabetic mice. According to the results, we found that the blood glucose and lipids in type 2 diabetes mice decreased significantly with SP treatment. SP was able to increase insulin sensitivity in diabetic mice and improve the intestinal microbiota composition of diabetic mice by the results of high throughput deep sequencing. The improvement of intestinal microbiota could play a vital role in reducing insulin resistance and blood glucose of diabetic mice. The results demonstrated that SP had ability to improve diabetic mellitus and owned the antidiabetic activity. As a consequence, SP could be a potential functional food for reducing blood glucose level and was expected to be suitable for applications in the food and pharmaceutical industries.

Study on Hypoglycemic Effect of Mulberry Leaf Extract Based on Big Data analysis

With the improvement of people’s living standards and the emergence of aging society, the incidence of diabetes is increasing year by year, and diabetes and its complications have become the third killer threatening human health. There are many drugs for treating diabetes, but their toxic and side effects are all great. Therefore, using big data analysis to find and develop natural products with hypoglycemic effect has high practical value. Therefore, the purpose of this paper is to study the hypoglycemic effect of mulberry leaf extract based on big data analysis. Firstly, this paper studies the medicinal value of mulberry leaves and related application methods by consulting relevant data. Through big data analysis, it is found that mulberry leaves are rich in alkaloid component 1-deoxynojirimycin (DNJ), accounting for more than 50% of alkaloid content. Therefore, this paper takes mulberry leaf extract DNJ as the research object, and firstly prepares mulberry leaf extract. Mulberry leaf water extract was perfused into stomach for 15 consecutive days, and fasting blood glucose of diabetic mice was measured 2 hours after eating by glucose oxidase method at specified time. The hypoglycemic effect of mulberry leaf water extract was analyzed by big data. The results showed that mulberry leaf extract could effectively inhibit the enzyme activity of decomposing sugar and prevent glucose absorption. Therefore, it can significantly reduce the blood sugar level of diabetic mice by about 50%. And the higher the dose of mulberry leaf extract, the better the hypoglycemic effect, showing a dose effect.