Metabolic Disorder Of Glucose Research Articles

Uncovering the function of insulin receptor substrate in termites' immunity through active immunization.

Insulin receptor substrate (IRS) proteins are key mediators in insulin signaling pathway. In social insect lives, IRS proteins played important roles in caste differentiation and foraging, but there function in disease defenses such as active immunization has not been reported yet. To investigate the issue, we successfully suppressed the IRS gene 3 days after dsRNA injection. Suppressing IRS gene increased the contents of glucose, trehalose, glycogen, and triglyceride and decreased the content of pyruvate in termites, and led to the metabolic disorder of glucose and lipids. IRS suppressing significantly enhanced grooming behaviors of nestmates of fungus-contaminated termites and hence increased the conidial load in the guts of the nestmates. Additionally, IRS suppressing led to significant downregulation of the immune genes Gram-negative bacteria-binding protein2 (GNBP2) and termicin and upregulation of the apoptotic gene caspase8, and hence diminished antifungal activity of nestmates of fungus-contaminated termites. The above abnormal behavioral and physiological responses significantly decreased the survival rate of dsIRS-injected nestmates of the fungus-contaminated termites. These findings suggest that IRS is involved in regulation of active immunization in termites, providing a better understanding of the link between insulin signaling and the social immunity of termites.

Lactational retrorsine exposure changes maternal milk components and disturbs metabolism homeostasis of offspring rats

Pyrrolizidine alkaloids (PAs) are a type of plant-derived environmental toxins, which pose a health hazard to human and livestock via contaminating soil, water, plants and food. In this study, we aimed to investigate the effect of lactational retrorsine (RTS, a typical toxic PA) exposure on breastmilk components and glucose-lipid metabolism of offspring rats. Dams were intragastrically administered with 5 mg/(kg·d) RTS during lactation. After metabolomic analyses, 114 differential constituents were identified in breastmilk between control and RTS groups, featured by reduction of lipids and lipid-like molecules, while presence of abundant RTS and its derivative in RTS-exposed milk. RTS exposure induced liver injury in pups, but the leakage of transaminases in serum recovered in their adulthood. Serum glucose levels were lower in pups but higher in male adult offspring from RTS group. RTS exposure also induced hypertriglyceridemia, hepatic steatosis and decreased glycogen content in both pups and adult offspring. Additionally, suppression of PPARα-FGF21 axis persisted in offspring liver after RTS exposure. These data indicated that inhibition of PPARα-FGF21 axis induced by milk deficient in lipid contents, together with hepatotoxic injury caused by RTS in breastmilk, may disrupt glucose and lipid metabolism of pups, and the persistent suppression of PPARα-FGF21 axis may program metabolic disorder of glucose and lipid in adult offspring.

The Complement System in Metabolic-Associated Kidney Diseases.

Metabolic syndrome (MS) is a group of clinical abnormalities characterized by central or abdominal obesity, hypertension, hyperuricemia, and metabolic disorders of glucose or lipid. Currently, the prevalence of MS is estimated about 25% in general population and is progressively increasing, which has become a challenging public health burden. Long-term metabolic disorders can activate the immune system and trigger a low-grade chronic inflammation named “metaflammation.” As an important organ involved in metabolism, the kidney is inevitably attacked by immunity disequilibrium and “metaflammation.” Recently, accumulating studies have suggested that the complement system, the most important and fundamental component of innate immune responses, is actively involved in the development of metabolic kidney diseases. In this review, we updated and summarized the different pathways through which the complement system is activated in a series of metabolic disturbances and the mechanisms on how complement mediate immune cell activation and infiltration, renal parenchymal cell damage, and the deterioration of renal function provide potential new biomarkers and therapeutic options for metabolic kidney diseases.

Short-term exposure to acrylamide exacerbated metabolic disorders and increased metabolic toxicity susceptibility on adult male mice with diabetes

Diabetes mellitus is a common endocrine metabolic disorder, and previous studies have shown that diabetics are more sensitive to the toxic environmental contaminants. Acrylamide (ACR) is both an industrially multipurpose compound and a common endogenous food contaminant to which people are frequently exposed and at high risk. However, the toxicity of ACR on diabetes hasn’t attracted much attention. In this study, both healthy mice and diabetic mice received ACR administration orally to investigate the ACR-induced metabolic toxicity, mechanism and susceptibility to ACR toxicity in adult diabetic male mice. The results showed that ACR significantly increased FBG level and decreased bodyweight, serum lipid and liver lipid biomarkers (TC, TG, LDL-C, HDL-C) levels as well as expression of lipid and glucose metabolism-related genes in diabetic mice, indicating that ACR can exacerbate metabolic disorders of glucose and lipid in diabetic male mice. Moreover, ACR exposure significantly increased levels of MDA and COX-2), decreased GSH level and antioxidant enzyme activity (SOD, GSH-PX and CAT) by downregulating expression of Nrf2 and Keap1 in diabetic mice. Factorial analysis showed ACR had a more significant disturbance in diabetic mice compared with healthy mice. Our results indicated that ACR exposure can cause oxidative stress and inflammatory damage, which can exacerbate abnormal glucose and lipid metabolism. This work helps to elucidate the effects and underlying mechanisms of ACR-induced metabolic toxicity in adults with diabetes.

Golden pompano (Trachinotus blochii) adapts to acute hypoxic stress by altering the preferred mode of energy metabolism

The golden pompano (Trachinotus blochii) is becoming increasingly popular among consumers for its delicate meat and high nutritional value. High farming density, eutrophication, and high-temperature conditions increase the probability of hypoxia and thus hypoxic stress, which poses a major challenge for the future development of golden pompano aquaculture. Here, we simulated severe hypoxic stress to distinguish hypoxia-tolerant and hypoxia-sensitive individuals from hundreds of fish. We then used next-generation sequencing to analyze the mRNA expression profiles of the brains and livers under hypoxia to identify the causes of differences in hypoxia tolerance among different groups. The pathways involved in highly expressed genes in the brain were mainly related to signal transduction, endocrine function, and environmental information processing, while the pathways involved in highly expressed genes in the liver were mainly related to metabolism. Under hypoxic conditions, the degradation of liver glycogen in the hypoxia-tolerant group was inhibited under hypoxia. However, in the hypoxia-intolerant group, glycogen decomposition is not inhibited, glucose consumption increases, and there is no tendency to convert to lipid metabolism, leading to metabolic disorders. In the process of adapting to hypoxia, fish first use anaerobic glycolysis to compensate for the lack of energy due to hypoxia. However, as the stress persists, glycolysis is inhibited, and lipid metabolism becomes the preferred mode of energy metabolism; specifically, acetyl-CoA may be produced through lipid metabolism in the hypoxia-tolerant group and then participate in the tricarboxylic acid cycle to provide energy. Death in the hypoxia-intolerant group may stem from the metabolic disorder of glucose and lipid homeostasis. Although additional research is needed to confirm these possibilities, our findings suggest that converting the preferred way of energy metabolism to lipid metabolism may be a way for fish to adapt to acute hypoxic stress.

The Metabolic Changes and Immune Profiles in Patients With COVID-19.

To explore the metabolic changes and immune profiles in patients with COVID-19, we analyzed the data of patients with mild and severe COVID-19 as well as young children with COVID-19. Of the leukocytes, 47% (IQR, 33–59) were lymphocytes [2.5 × 109/L (IQR, 2.2–3.3)], and monocytes were 0.51 × 109/L (IQR, 0.45–0.57) in young children with COVID-19. In 32 mild COVID-19 patients, circulating monocytes were 0.45 × 109/L (IQR, 0.36–0.64). Twenty-one severe patients had low PO2 [57 mmHg (IQR, 50–73)] and SO2 [90% (IQR, 86–93)] and high lactate dehydrogenase [580 U/L (IQR, 447–696)], cardiac troponin I [0.07 ng/mL (IQR, 0.02–0.30)], and pro-BNP [498 pg/mL (IQR, 241–1,726)]. Serum D-dimer and FDP were 9.89 mg/L (IQR, 3.62–22.85) and 32.7 mg/L (IQR, 12.8–81.9), and a large number of RBC (46/μL (IQR, 4–242) was presented in urine, a cue of disseminated intravascular coagulation (DIC) in severe patients. Three patients had comorbidity with diabetes, and 18 patients without diabetes also presented high blood glucose [7.4 mmol/L (IQR, 5.9–10.1)]. Fifteen of 21 (71%) severe cases had urine glucose +, and nine of 21 (43%) had urine ketone body +. The increased glucose was partially caused by reduced glucose consumption of cells. Severe cases had extraordinarily low serum uric acid [176 μmol/L (IQR, 131–256)]. In the late stage of COVID-19, severe cases had extremely low CD4+ T cells and CD8+ T cells, but unusually high neutrophils [6.5 × 109/L (IQR, 4.8–9.6)], procalcitonin [0.27 ng/mL (IQR, 0.14–1.94)], C-reactive protein [66 mg/L (IQR, 25–114)] and an extremely high level of interleukin-6. Four of 21 (19%) severe cases had co-infection with fungi, and two of 21 (9%) severe cases had bacterial infection. Our findings suggest that, severe cases had acute respiratory distress syndrome (ARDS) I–III, and metabolic disorders of glucose, lipid, uric acid, etc., even multiple organ dysfunction (MODS) and DIC. Increased neutrophils and severe inflammatory responses were involved in ARDS, MODS, and DIC. With the dramatical decrease of T-lymphocytes, severe cases were susceptible to co-infect with bacteria and fungi in the late stage of COVID-19. In young children, extremely high lymphocytes and monocytes might be associated with the low morbidity of COVID-19. The significantly increased monocytes might play an important role in the recovery of patients with mild COVID-19.

Correlation Between Serum PON1 Arylesterase Activity and Rs 854573 <i>PON1 A < G</i> Polymorphism with Type 2 Diabetes in an Eastern Indian Cohort

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder of glucose and lipids and characterized by defect in insulin secretion or action. Oxidative imbalance has also been implicated in the etiology of diabetes. Paraoxonase-1 (PON1) is an esterase and lactonase which is found in the circulation bound to high-density lipoproteins (HDL). Alterations and associations of circulating PON1 levels with a variety of diseases including diabetes encourages us to investigate the possible association between PON1 A/G rs854573 polymorphism and serum PON1 activity with T2DM. The study essentially follows a population based case-control format with 101 diabetic and 102 healthy controls. The findings revealed association of polymorphism with the diseased status (p value 0.0002, OR 3.49, 95% CI 1.77 to 6.9). With significantly higher range of mean serum PON1 Arylesterase (AREase) activity in control (9.99 – 0.96 kU/L) than in diabetic patients (5.25 - 0.508 kU/L) (p value,<0.001), a large difference between common diabetic AA genotype and combined diabetic heterozygous and homozygous genotypes (AG+GG) for risk allele G (assymptometic p value,<0.001), or in between two AA genotypes (Diabetic/Non diabetic, p<0.001), was explored by parametric and non parametric statistical pairwise comparison. Serum PON1 activity was found to be independent of other clinical factors such as plasma glucose levels. Western blot analysis of serum samples detected a significant difference of PON1 proteins in diabetic patients and control subjects (p value 0.008). In conclusion serum PON1 AREase activity which to an extent correlated with PON1 promoter polymorphism might be a good predictor of the disease risk.

Sulfonylureas Induced Hypoglycemia in Diabetics - A Review

Diabetes is a metabolic disorder of glucose characterized by glucotoxicity, lipotoxicity and insulin resistance. In insulin resistance states, a higher level of insulin is needed to generate the usual body response to keep plasma glucose at physiologic level. The type 2 diabetics with insulin resistance cannot keep plasma glucose normal not because of absolute insulin deficiency but due to a relative deficiency as insulin is now required at a higher plasma level to achieve a near physiological or physiological plasma glucose level. Hence the need for a chemical agent to increase insulin secretion from the pancreatic beta cells at pharmacological dose (insulin secretagogues) was conceptualized and arrived at. Sulfonylureas are insulin secretagogues. Two generations of sulfonylurea’s are in use. The first and second. The class effects of sulfonylurea include weight gain, allergic reaction and hypoglycemia. But not enough emphasis is placed on the severity and grading of the hypoglycemia complicating use of sulfonylureas. Meanwhile hypoglycemia induced by sulfonylurea use is of various degree, severity and duration. The classification of hypoglycemia into grades in ADEMOLUS CLASSIFICATION OF HYPOGLYCEMIA makes it easier for scientist to understand, compare and monitor the severity of sulfonylureas. Mrs KFO is a 67 years old diabetic diagnosed over 8 years ago. She had asymptomatic hypoglycemia with a glucometer reading low (ADEMOLUS PHENOMENON) on a clinic day visit. She had been on glimepiride for three years. Mrs A. F. is a 75 years old diabetic diagnosed 4 years prior to presentation. She had a glucometer reading of low during a random blood sugar check at 8pm on day 2 of admission with associated general body weakness. She was on metformin and glibenclamide. Mrs. I E is a 72 years old diabetic who had a glucometer reading of low during her outpatient clinic visit. She was on gliclazide. Sulfonylureas use has been shown by these cases to be associated with symptomatic and asymptomatic very severe hypoglycemia. A possibility of synthesizing a new equally potent third generation of sulfonylureas with minimal or no hypoglycemic effect should be looked into.

An investigation of the association between the level of prolactin in serum and type II diabetes

As a hormone secreted from the pituitary gland, prolactin (PRL) plays an important role in increasing beta cell proliferation, stimulating the secretion of insulin, preventing the activities of caspases on pathways that cause apoptosis in the Langerhans' islands, and moderating the immune system in regulating the whole body's sensitivity to insulin. Therefore, PRL level changes in type II diabetes and it can be concluded that PRL can play an important role in metabolic disorders of glucose. The present study is carried out in order to investigate the association between serum levels of PRL and type II DM. Blood samples were taken from 64 females affected by type II diabetes and 70 healthy ones, whose PRL level was measured using electrochemiluminescence (ECL) technique. It was a case-control study, and based on the definition dedicated to each group, subjects were assigned to two groups. The patient group included the subjects with type II diabetes while the control group included healthy samples. Data were analyzed using SPSS software (Mann-Whitney test, t-test, and spearman's rho correlation test). According to the results, PRL concentration in the serum of people affected by type II diabetes (5.32 ± 0.36) was significantly (P˂0.05) lower than that of control group (18.38 ± 2.3). The results also showed that in type II diabetes, the level of PRL changes so that the concentration of PRL in the serum of the patients was lower than that of healthy ones. Therefore, PRL concentration in the blood can be related to diabetes.

Insulin delivery systems combined with microneedle technology.

Diabetes, a metabolic disorder of glucose, is a serious chronic disease and an important public health problem. Insulin is one of the hormones for modulating blood glucose level and the products of which is indispensable for most diabetes patients. Introducing microneedles (MNs) to insulin delivery is promising to pave the way for modulating glucose level noninvasively of diabetes patients, as which born to be painless, easy to handle and no need of any power supply. In this work, we review the process of insulin delivery systems (IDSs) based on MN technology in terms of two categories: drug free MNs and drug loaded MNs. Drug free MNs include solid MNs ("poke and patch"), hollow MNs ("poke and flow") and reservoir-based swelling MNs ("poke and swell R-type"), and drug loaded MNs include coated MNs ("coat and poke"), dissolving MNs ("poke and release") and insulin incorporated swelling MNs ("poke and swell I-type"). Majority researches of MN-based IDSs have been conducted by using hollow MNs or dissolving MNs, and almost all clinical trials for MN-based IDSs have employed hollow MNs. "Poke and patch" approach dramatically increase skin permeability compared to traditional transdermal patch, but MNs fabricated from silicon or metal may leave sharp waste in the skin and cause a safety issue. "Poke and flow" approach, similar to transitional subcutaneous (SC) injection, is capable of producing faster insulin absorption and action than SC injection but may associate with blockage, leakage and low flow rate. Coated MNs are able of retaining the activity of drug, which loaded in a solid phase, for a long time, however have been relatively less studied for insulin application as the low drug dosing. "Poke and release" approach leaves no biohazardous sharp medical waste and is capable of rapid drug release. "Poke and swell R-type" can be seen as a combination of "poke and flow" and "poke and patch" approach, while "poke and swell I-type" is an approach between "coat and poke" and "poke and release" approach. Insulin MNs are promising for painless diabetes therapeutics, and additional efforts for addressing fundamental issues including the drug loading, the PK/PD profile, the storage and the safety of insulin MNs will accelerate the clinical transformation.

Effect of curcumin on glucose and lipid metabolism, FFAs and TNF-α in serum of type 2 diabetes mellitus rat models

ObjectiveTo investigate how curcumin affects the glucose and lipid metabolism in type 2 diabetes mellitus (DM) rat models, and to explore its effect on the free fatty acid (FFA) and tumor necrosis factor α (TNF-α) in serum.MethodsSuccessfully established type 2 DM rats were divided into three groups, i.e. the normal control group, model group and curcumin group, and received the medication for consecutive 8 weeks. Thereafter, we detected the level of fasting blood glucose (FBG), and the blood glucose at 30 min, 60 min and 120 min; besides, we also carried out the insulin tolerance tests to measure the levels of fasting serum insulin (FINS) and blood glucose at 40 min and 90 min; additionally, we also detected the levels of TC, TG, HDL-C, LDL-C, FFA and TNF-α in serum. The results were expected to discover the mechanism of curcumin in decreasing the blood glucose level in DM rats.ResultsCompared with the model group, AUCs of FBG, blood glucose at 30 min, 60 min and 120 min, and glucose were decreased in varying degrees in the curcumin group, and the differences had statistical significance (p < .05). After subcutaneous injection of insulin, we found that the blood glucose at 40 min and 90 min in the curcumin group was decreased, while AUC of glucose level was also decreased (p < .05 or .01). Eight weeks after medication, compared with the rats in the normal group, the levels of HDL-C, LDL-C, TC and TG in rats of the model group and the curcumin group were obviously increased (p < .05). In comparison with the model group, the level of LDL-C in rats of the curcumin group was also decreased significantly (p < .05). In comparison with the normal control group in the same period, we found that the content of FFAs and TNF-α in serum of rats of the model group were elevated significantly, and the differences had statistical significance (p < .05 or .01); the levels in the curcumin group were significantly decreased in comparison with the model group in the same period, and the difference had statistical significance (p < .05 or .01).ConclusionTreatment with curcumin can significantly improve the metabolic disorder of glucose and lipid, enhance the sensitivity to the insulin, and ameliorate the resistance to insulin of the type II DM rats. Meanwhile, this treatment method can also significantly decrease the level of FFA and TNF-α in serum of type II DM rats. Thus, we inferred that the mechanism of curcumin to improve the insulin resistance might be correlated with the decreases of FFA and TNF-α in serum.

Pancreatic atrophy caused by dietary selenium deficiency induces hypoinsulinemic hyperglycemia via global down-regulation of selenoprotein encoding genes in broilers.

This study was envisaged to comprehensively profile genes in selected tissues along with a few biochemical indicators and integrate resulting information with dietary selenium (Se) deficiency symptoms in broilers. A total of 120 one-day-old Cobb male broilers were equally divided into two groups and fed a Se deficient corn-soybean-based basal diet supplemented with 0.3 mg/kg sodium selenite (Control, Se adequate) or without selenite (Se deficiency) for five weeks. Effects of Se deficiency on mRNA abundance of twenty-three selenoprotein encoding genes and seventeen insulin signaling related genes were studied at day 35 in pancreas, liver and muscle along with plasma biochemical constituents and enzyme activities. Compared to healthy birds in control diet, Se deficient diet induced deficiency symptoms in 90% birds and classic nutritional pancreatic atrophy, depressed growth performance of broilers, and decreased (P < 0.01 to P < 0.05) total antioxidant capacity and activities of superoxide dismutase and glutathione peroxidase in plasma and three other tissues. Se deficiency resulted in 58% higher mortality than control birds. Dietary Se deficiency down-regulated (P < 0.01–0.05) eighteen selenoprotein encoding genes in pancreas, fourteen genes in muscle and nine genes in liver, and up-regulated (P < 0.05) Txnrd1 and Selx in liver. Meanwhile, six, thirteen and five insulin signaling related genes were down-regulated (P < 0.01–0.05) in pancreas, muscle and liver, respectively, and three genes were up-regulated (P < 0.01) in liver. The decrease (P < 0.05) in levels of plasma insulin, total triglyceride and total cholesterol, and concurrent elevated (P < 0.05) levels of plasma glucose and inflammatory cytokines accompanied the global down-regulation of selenoprotein encoding- and insulin signaling related- genes in Se deficient birds. It was concluded that dietary Se deficiency induces nutritional pancreatic atrophy and metabolic disorder of glucose and lipid in broilers via down-regulation of selenoprotein encoding- and insulin signaling related- genes, indicating potential roles of these genes in metabolic regulation.

PPAR-gamma Signaling in Metabolic Homeostasis

BACKGROUND: Peroxisome proliferator-activated receptor (PPAR)-γ, or also known as nuclear receptor subfamily 1 group C member 3 (NR1C3), is a PPAR which serves as master regulator of adipocytes differentiation, and plays an important role in lipid metabolism or adipogenesis. Recent study showed that PPAR-γ is expressed in most tissue and also has critical impact in many metabolic homeostasis disorders.CONTENT: Dysregulation of PPAR-γ is correlated to the development of obesity, type 2 diabetes, atherosclerosis, cardiovascular disease, acute kidney injury, autoimmune disease, gastrointestinal disease and Alzheimer’s disease. Abundant number of new emerging compounds, with in vitro and in vivo effectiveness as natural and synthetic agonists of PPARs, are investigated, developed and used as the treatment of metabolic disorders of glucose and/or lipid and other diseases.SUMMARY: Based on all studies explanation, targeting PPAR-γ is proven to be a good therapeutic method for reducing negative effect of several metabolic homeostasis disorder. Now, many natural and synthetic agonists of PPARs are used as the treatment of metabolic disorders of glucose and/or lipid or another metabolic homeostasis disorder. Such agonists have different properties and specificities for individual PPARs receptors, different absorption and distribution, and distinctive gene expression profiles, which ultimately lead to different clinical outcomes.KEYWORDS: PPAR-γ, dysregulation, agonist, adipogenesis, metabolic disorder, homeostasis

Research progress of mechanism of vitamin D in regulating obesity and insulin resistance on children

Vitamin D has a wide range of biochemical effects.Insufficiency/deficiency of vitamin D increases the risk of insulin resistance by ways of inflammation, adipocytokines, oxidative stress and mitochondria function, it could lead to metabolic disorder of glucose and lipid, which closely relates to the incidence and development of obesity and metabolic syndrome on children.This paper presents the relationship between vitamin D with obesity and metabolic syndrome on children, states the possible mechanisms of regulation of glucose/lipid metabolism and insulin resistance by vitamin D. Key words: Vitamin D; Child; Obesity; Adipocytokine; Insulin resistance

Spontaneous rupture of adrenal incidentaloma in a patient with subclinical Cushing’s syndrome, whose clinical expression is metabolic syndrome

A 68-year-old female with enlarged bilateral adrenal glands who was being monitored for metabolic syndrome (MetS) and subclinical Cushing’s syndrome was admitted to our hospital because of rupture of the left adrenal gland. We performed abdominal aortography and embolization of the left middle adrenal artery, and the patient’s pain resolved soon afterwards. After the left adrenal rupture, endocrinological studies still showed subclinical Cushing’s syndrome, and she exhibited no changes in the metabolic disorders. Because she refused removal of the left adrenal gland, we observed her clinical course carefully. One year after the adrenal gland rupture, abdominal computed tomography revealed complete absorption of the retroperitoneal hemorrhage and 131I-adosterol scintigraphy showed a similar result to that previously found. Although adrenal rupture is a rare condition, we should be aware of its possibility during the follow-up of incidental adrenal tumors. Subclinical Cushing’s syndrome has many common features with lifestyle diseases, such as excessive visceral fat, hypertension, metabolic disorders of glucose and lipids. Careful examinations are needed to follow up many patients with lifestyle-related diseases or MetS for a long period.

α-Tocopherol status and altered expression of α-tocopherol-related proteins in streptozotocin-induced type 1 diabetes in rat models.

Vitamin E plays a critical role as an antioxidant in several pathological conditions, including diabetes, cancer, cardiovascular diseases, and neurodegenerative disorders. Diabetes is a metabolic disorder of glucose due to the lack of adequate insulin production (type 1) or peripheral insulin resistance (type 2). Oxidative stress plays a major role in the pathogenesis of diabetes and its complications. The purpose of the present study was to determine α-tocopherol status and the expression of α-tocopherol-related proteins, including binding proteins and metabolizing enzymes, under streptozotocin (STZ)-induced type 1 diabetes in rat models. In STZ rats, plasma α-tocopherol levels decreased compared to the control rats, whereas hepatic α-tocopherol levels in the STZ rats were significantly increased. CuZn-superoxide dismutase (SOD) gene expression in the liver of STZ rats was markedly decreased, whereas Mn-SOD gene expression remained unaltered. Accelerated lipid peroxidation in the liver of STZ rats was observed and the hepatic expression of α-tocopherol transfer protein (α-TTP) in STZ rats decreased compared to that in the controls. The hepatic expression of cytochrome P450 4F2 (CYP4F2) and CYP3A2 genes in STZ rats also decreased. The reduced expression of hepatic α-TTP and CYP4F2 genes probably leads to decreased plasma α-tocopherol levels and elevated α-tocopherol levels in the liver of STZ rats. The altered expression of hepatic α-tocopherol-related proteins might regulate α-tocopherol status in type 1 diabetes. Determining the mechanism of modulating α-tocopherol status may be helpful in promoting antioxidant therapy in diabetes.

Comparative study on effection of risperidone to the metabolism in schizophrenia patients

Objective To explore the affection and related factors of risperidone on the metabolic indexes in schizophrenia patients.Methods 56 cases hospitalized schizophrenia patients were treated with risperidone for 16 weeks.Waistline,blood glucose and blood lipid,blood pressure and other indicators were observed before and after treatment,risk factors that caused metabolic syndrome (MS) and abnormal indexes were analyzed,and 36 healthy persons as control group.Results The rate of MS in patient group was obviously higher than that in control group ( 12.50％ vs 0％,P =0.026).Waistline,triglyceride ( TG),high density lipoprotein ( HDL-C ),and 2 hours postprandial blood glucose (2hPG) in patient group ( (4.15 ± 3.14)cm in man and (4.41 ± 2.86)cm in woman,(0.26 ±0.51 ) mmol/L,(-0.09 ±0.19) mmol/L,(0.49 ±0.84) mmol/L) increased compared with that in control group ( ( 0.76 ± 1.09 ) cm in man and ( 0.64 ± 0.81 ) cm in woman,( 0.04 ± 0.15 ) mmol/L,(-0.01 ± 0.12)mmol/L,(0.04 ± 0.35 ) mmol/L) at the 16th weekend,and difference was significantly (P ＜ 0.05 ).Logistic regression analysis showed that the risk factors were family history of diabetes Odds Ratio (OR) 20.34 (95％ CI 1.97 ～210) and age OR 1.19(95％CI 1.03 ～ 1.38),the basis waistline OR 1.26 (95％ CI 1.04 ～ 1.52) and family history of obesity OR 4.27(95％ CI 1.21 ～ 15.1 ),the basis TG OR 73.88 (95％ CI 3.41 ～ 16.01 ) and the basis systolic pressure OR 1.16 (95％ CI 1.00 ～ 1.33 ),the basis waistline OR 1.41 (95 ％ CI 1.08 ～ 1.84 ) and age OR 1.53 (95％ CI 1.02 ～ 1.31 ) in developed MS,abnormal rate of waistline,TG,and 2hPG.Conclusion Risperidone can cause abdominal obesity,metabolic disorders of glucose and lipid even MS.So it shoud be used carefully for the patient who is old and has family history of diabetes and obesity posture. Key words: Risperidone; Schizophrenia; Metabolic indexes; Metabolic syndrome

Prevention and treatment of metabolic syndrome with integrated traditional Chinese and Western medicine

Metabolic syndrome also can be named insulin resistance syndrome. The main clinical manifestations include metabolic disorders of glucose and lipid and some diseases caused by the metabolic disorder, such as impaired glucose tolerance or diabetes, obesity, hyperlipemia, fatty liver, hypertension, coronary heart disease, microalbuminuria, etc. According to the theory of zang-fu organs (viscera) in traditional Chinese medicine, these diseases all result from the deficiency of spleen-qi. They are characterized by deficiency in the Ben (root) and excess in the Biao (branch). The Ben (root) is the failure of the spleen in transportation, and the Biao (branch) is stagnation of qi, blood, phlegm, fire, dampness and food. In the prevention and treatment of metabolic syndrome, it is advocated that the intervention of medicine should be used as early as possible, so as to slow down the occurrence and development of insulin resistance, and that emphasis should be transferred from decreasing blood glucose alone to comprehensive prevention of risk factors, especially to the prevention of cardiovascular events. The effect of traditional Chinese herbs is not as good as the western drugs in decreasing the blood pressure and glucose. However, the traditional Chinese herbs have distinctive superiority in ameliorating the insulin resistance, protecting the injury of vascular endothelial cells, regulating the metabolism of lipid, inhibiting the hypercoagulability, and treating the inflammation. Moreover, they are relatively safe. Therefore, the integration of the traditional Chinese medicine and western medicine is worth further research.

Background of cardiovascular diseases in adult--with special reference to metabolic disorder of glucose and hypertension

Background of cardiovascular diseases in adult--with special reference to metabolic disorder of glucose and hypertension