Glucose Transport Mechanism Research Articles

Structure and mechanism of a phosphotransferase system glucose transporter

Glucose is the primary source of energy for many organisms and is efficiently taken up by bacteria through a dedicated transport system that exhibits high specificity. In Escherichia coli, the glucose-specific transporter IICBGlc serves as the major glucose transporter and functions as a component of the phosphoenolpyruvate-dependent phosphotransferase system. Here, we report cryo-electron microscopy (cryo-EM) structures of the glucose-bound IICBGlc protein. The dimeric transporter embedded in lipid nanodiscs was captured in the occluded, inward- and occluded, outward-facing conformations. Together with biochemical and biophysical analyses, and molecular dynamics (MD) simulations, we provide insights into the molecular basis and dynamics for substrate recognition and binding, including the gates regulating the binding sites and their accessibility. By combination of these findings, we present a mechanism for glucose transport across the plasma membrane. Overall, this work provides molecular insights into the structure, dynamics, and mechanism of the IICBGlc transporter in a native-like lipid environment.

Glucose stockpile in the intestinal apical brush border in C. elegans

Revealing the mechanisms of glucose transport is crucial for studying pathological diseases caused by glucose toxicities. Numerous studies have revealed molecular functions involved in glucose transport in the nematode Caenorhabditis elegans, a commonly used model organism. However, the behavior of glucose in the intestinal lumen-to-cell remains elusive. To address that, we evaluated the diffusion coefficient of glucose in the intestinal apical brush border of C. elegans by using fluorescent glucose and fluorescence recovery after photobleaching. Fluorescent glucose taken in the intestine of worms accumulates in the apical brush border, and its diffusion coefficient of ∼10−8 cm2/s is two orders of magnitude slower than that in bulk. This result indicates that the intestinal brush border is a viscous layer. ERM-1 point mutations at the phosphorylation site, which shorten the microvilli length, did not significantly affect the diffusion coefficient of fluorescent glucose in the brush border. Our findings imply that glucose enrichment is dominantly maintained by the viscous layer composed of the glycocalyx and molecular complexes on the apical surface.

Глюкозні транспортери сімейства GLUT у патогенезі проліферативної діабетичної ретинопатії пацієнтів із цукровим діабетом 2-го типу

The supply of glucose to neurons of the brain and retina is carried out by a specific, facilitated transport with the participation of sodium-independent glucose transporters of the GLUT family. Studying the mechanisms of glucose transport with pharmacological or genetic inhibition of transporters is considered as a promising way to reduce glucose-toxic damage to the retina to prevent diabetic retinopathy. We studied the content of GLUT1, GLUT3, GLUT4 and Hypoxia inducible factor 1 alpha (HIF-1α) in the plasma of patients with different stages of proliferative diabetic retinopathy (PDR), duration of type 2 diabetes (T2D) was up to 20 and over 20 years, and control group. Research on the level of transporters in the blood plasma was carried out by the method of immuno-enzymatic analysis using Elabscience kits (USA). No significant difference in the GLUT1 and GLUT4 blood plasma content was found between patients with PDR and control individuals, and the GLUT3 content was 2-fold higher. Also, the content of HIF-1α was 25% higher. No significant fluctuations in the content of transporters GLUT1, GLUT3, GLUT4, HIF-1α were found depending on the duration of T2DM, the degree of deepening of PDR and the level of hyperglycemia. Correlation analysis revealed a significant two-way correlation of the GLUT3 index with blood glucose level (r = 0.581), HbA1C (r = 0.553), GLUT1 (r = 0.440) and GLUT4 (r = 0.372). The conservatism of GLUT1 transporter content in the studied groups gives a reason to consider protein expression as genetically determined for the basic maintenance of homeostasis. The GLUT3 content increase in patients with PDR, which does not depend on the retinal damage degree, duration of T2D and glucose concentration, defines this mechanism of transport as the main pathogenetic link of glucose toxicity in neurons against the background of chronic hyperglycemia. Insulin-dependent transporter GLUT4 is probably not involved in the occurrence of PDR under of T2D.

Conditioning-induced expression of novel glucose transporters in canine skeletal muscle homogenate.

Athletic conditioning can increase the capacity for insulin-stimulated skeletal muscle glucose uptake through increased sarcolemmal expression of GLUT4 and potentially additional novel glucose transporters. We used a canine model that has previously demonstrated conditioning-induced increases in basal, insulin- and contraction-stimulated glucose uptake to identify whether expression of glucose transporters other than GLUT4 was upregulated by athletic conditioning. Skeletal muscle biopsies were obtained from 12 adult Alaskan Husky racing sled dogs before and after a full season of conditioning and racing, and homogenates from those biopsies were assayed for expression of GLUT1, GLUT3, GLUT4, GLUT6, GLUT8, and GLUT12 using western blots. Athletic conditioning resulted in a 1.31 ± 0.70 fold increase in GLUT1 (p <0.0001), 1.80 ± 1.99 fold increase in GLUT4 (p = 0.005), and 2.46 ± 2.39 fold increase in GLUT12 (p = 0.002). The increased expression of GLUT1 helps explain the previous findings of conditioning-induced increases in basal glucose clearance in this model, and the increase in GLUT12 provides an alternative mechanism for insulin- and contraction-mediated glucose uptake and likely contributes to the substantial conditioning-induced increases in insulin sensitivity in highly trained athletic dogs. Furthermore, these results suggest that athletic dogs can serve as a valuable resource for the study of alternative glucose transport mechanisms in higher mammals.

Early-life influences of low-calorie sweetener consumption on sugar taste

Children and adolescents are the highest consumers of added sugars, particularly from sugar-sweetened beverages (SSB). Regular consumption of SSB early in life induces a variety of negative consequences on health that can last into adulthood. Low-calorie sweeteners (LCS) are increasingly used as an alternative to added sugars because they provide a sweet sensation without adding calories to the diet. However, the long-term effects of early-life consumption of LCS are not well understood. Considering LCS engage at least one of the same taste receptors as sugars and potentially modulate cellular mechanisms of glucose transport and metabolism, it is especially important to understand how early-life LCS consumption impacts intake of and regulatory responses to caloric sugars. In our recent study, we found that habitual intake of LCS during the juvenile-adolescence period significantly changed how rats responded to sugar later in life. Here, we review evidence that LCS and sugars are sensed via common and distinct gustatory pathways, and then discuss the implications this has for shaping sugar-associated appetitive, consummatory, and physiological responses. Ultimately, the review highlights the diverse gaps in knowledge that will be necessary to fill to understand the consequences of regular LCS consumption during important phases of development.

Magnesium deficiency as a contributing factor to type 2 diabetes: a review of the literature

Magnesium deficiency is a vital contributing factor to the happening and arising of insulin resistance, metabolic syndrome, and type 2 diabetes mellitus. Magnesium has a critical function in controlling the level of glucose in the blood and insulin sensitivity, acting as a cofactor for various enzymes such as enzymes involved in carbohydrate oxidation, glucose transport mechanisms of the cell membrane, cell replication, and lipid metabolism. Studies have indicated that reduced magnesium levels in the blood are connected with a significant decline in insulin-mediated glucose uptake which is a vital part of the cell’s metabolism. In people with type 2 diabetes, plasma magnesium concentration was inversely associated with markers of insulin resistance. This means as magnesium levels in plasma decrease, the risk of insulin resistance increases. Additionally, magnesium deficiency can play a role in the development of diabetes by affecting the activity of the Na/K-ATPase enzyme, pancreas inflammation, reactive oxygen species (ROS) modification, lipid metabolism, and causing genetic instability, as the main contributors to type 2 diabetes. Therefore, early detection of magnesium deficiency can help prevent further complications. Physicians should be aware of the connection between magnesium deficiency and diabetes and monitor patients with magnesium deficiency for diabetes symptoms and make sure that the patient is getting adequate amounts of magnesium from their diet. Further research is needed to reveal the exact mechanisms underlying magnesium deficiency-induced type 2 diabetes and the curative effects of magnesium supplementation.

Positive correlation of psoriasis vulgaris severity and HOMA-IR

Background: Psoriasis vulgaris is a chronic inflammatory skin disease that its aetiology is still not completely known. A chronic inflammation in psoriasis can cause organ dysfunctions. Elevation of proinflammatory cytokines gives rise to insulin resistance by inhibiting insulin and glucose transport mechanism signals. Insulin resistance is the underlying pathogenesis of metabolic syndrome.&#x0D; Objective: This study aimed to undestand any correlation in the severity of psoriasis vulgaris with HOMA-IR.&#x0D; Methods: A cross sectional research involving 35 subjects with psoriasis vulgaris and 15 subjects without who met the selection criteria. HOMA-IR is a formula used to measure insulin resistance which calculates the fasting insulin value in μU/ml x fasting glucose in mg/DL/405 taken from the blood veins of subjects. PASI score was used to determine psoriasis vulgaris severity.&#x0D; Results: This study shows that the HOMA-IR median value was higher in psoriasis subject than the subjects without psoriasis (p&lt;0.05). The correlaton analysis shows a moderate positive correlation between psoriasis vulgaris severity and HOMA-IR (r= 0.427; p&lt;0.05). The prevalence ratio was 8.57, which means psoriasis vulgaris subjects were 8.57 times more likely to have HOMA-IR compared to those without psoriasis vulgaris (p&lt;0.05; 95%CI: 1.26-58.1).&#x0D; Conclusion: This study concludes that there is a moderate positive correlation between severity of psoriasis vulgaris and HOMA-IR values.

Muscle-Specific Ablation of Glucose Transporter 1 (GLUT1) Does Not Impair Basal or Overload-Stimulated Skeletal Muscle Glucose Uptake.

Glucose transporter 1 (GLUT1) is believed to solely mediate basal (insulin-independent) glucose uptake in skeletal muscle; yet recent work has demonstrated that mechanical overload, a model of resistance exercise training, increases muscle GLUT1 levels. The primary objective of this study was to determine if GLUT1 is necessary for basal or overload-stimulated muscle glucose uptake. Muscle-specific GLUT1 knockout (mGLUT1KO) mice were generated and examined for changes in body weight, body composition, metabolism, systemic glucose regulation, muscle glucose transporters, and muscle [3H]-2-deoxyglucose uptake ± the GLUT1 inhibitor BAY-876. [3H]-hexose uptake ± BAY-876 was also examined in HEK293 cells-expressing GLUT1-6 or GLUT10. mGLUT1KO mice exhibited no impairments in body weight, lean mass, whole body metabolism, glucose tolerance, basal or overload-stimulated muscle glucose uptake. There was no compensation by the insulin-responsive GLUT4. In mGLUT1KO mouse muscles, overload stimulated higher expression of mechanosensitive GLUT6, but not GLUT3 or GLUT10. In control and mGLUT1KO mouse muscles, 0.05 µM BAY-876 impaired overload-stimulated, but not basal glucose uptake. In the GLUT-HEK293 cells, BAY-876 inhibited glucose uptake via GLUT1, GLUT3, GLUT4, GLUT6, and GLUT10. Collectively, these findings demonstrate that GLUT1 does not mediate basal muscle glucose uptake and suggest that a novel glucose transport mechanism mediates overload-stimulated glucose uptake.

Implication of SMIT1 in ROS-dependent alteration of endothelial function during an acute hyperglycemia

Previous investigations from our group and others revealed that hyperglycemia (HG) impairs vascular endothelial function particularly through an increased oxidative stress. For a long time, little was known about the glucose transport mechanisms responsible for these alterations in the cardiovascular system under HG conditions. However, recent work has shown the involvement of the sodium myo-inositol transporter 1 (SMIT1) of the sodium-glucose co-transporter (SGLT) family in HG-dependent ROS production. However, few studies have focused on the involvement of these transporters in the vascular effects of HG. In this context, we aimed to evaluate the implication of the different SGLT isoforms on the increased oxidative stress and the subsequent vascular dysfunction reported during HG. Firstly, Gene expression of the 7 isoforms of SGLT Transporters was evaluated in vascular tissues by PCR. Then, in order to study the involvement of SGLT/SMIT transporters in HG-related vascular alterations, we incubated (1 hour, 100 mM) aortic rings from Wistar rats with either of the following sugars which each stimulate either one or more isoforms of these transporters (Glucose: GLUTs/SGLTs/SMITs transporters; α-MG: SGLT 1 to 5; Galactose: SGLT 1/2; myo-inositol: SMIT 1/2; L-Fucose: SMIT1). Then, incubated vessels were either mounted in organ chambers to study vascular endothelial function or embedded in OCT in order to measure reactive oxygen species (ROS) production with DHE fluorescence. First, PCR analyses highlighted that SMIT1 appears to be the transporter of the SGLT family whose gene expression is predominant in vascular tissue. As expected from previous studies, vascular exposure to glucose was responsible for an endothelial dysfunction associated with a higher ROS production. Interestingly, endothelial impairments and increased ROS production were not observed when SGLTs were stimulated with either α-MG or galactose. The main result of this work was that myo-inositol exposure was responsible for similar endothelial alteration than glucose and that L-Fucose which transport is highly dependent of SMIT1 was responsible for an exacerbation of those impairments. These results highlight the implication of SMIT1 in the increased oxidative stress and endothelial dysfunctions observed during HG in vascular tissues.

Study of Serum Magnesium Level in Type 2 Diabetes Mellitus in Relation to Its Microvascular Complication

Magnesium is an essential element and has a fundamental role in carbohydrate metabolism in general and in the insulin action in particular. Magnesium is a cofactor in both glucose transport mechanism of the cell membranes and for various intracellular enzymes involved in carbohydrate oxidation the concentrations of magnesium in serum of healthy people are remarkably constant, whereas 25-39% of diabetics have low concentrations of serum magnesium. Magnesium depletion has a negative impact on glucose homeostasis and insulin sensitivity in patients with type 2 diabetes, as well as on the evolution of complications such as ischemic heart disease, arterial atherosclerosis, hypercholesterolemia, hyper triglyceridemia, hypertension, retinopathy, neuropathy and nephropathy. Moreover, low serum magnesium is a strong, independent predictor of development of type 2 diabetes. The study is one and half year observational comparative hospital based study conducted in patients attending the Medicine OPD. Randomly chosen 100 Type 2 diabetic patients, and 100 non diabetic age/sex matched controls were included. In this study significant correlation is found between Hypomagnesemia and Diabetic Retinopathy. Diabetes Mellitus Type 2 with Hypomagnesemia is associated with more microvascular complications. Serum Magnesium level also found to be correlated with Lipid profile in Diabetics and significant correlation was also found between Hypomagnesemia and Hypertension. Keywords: Serum Magnesium Level, Type 2 Diabetes Mellitus, Microvascular Complication.

L-Arginine’s Glucose Homeostatic Influence in Renal Damaged Wistar Rats is Possibly Mediated by Adiponectin Expression

Hypoglycemia, as a direct result of the glucosuria is usually seen in patients with acute kidney injury hence glucose homeostasis is disturbed. The compensatory effect of adiponectin in the insulin deficient state is documented. We previously demonstrated that L-arginine enhances glucose transport mechanisms in renal-damaged rats. The current study was designed to investigate possible glucose handling synergy between L-arginine and adiponectin in Wistar rats induced with acute kidney injury. Twenty four rats weighing between 120g-150g were divided into 4 groups of six rats each. Group 1 (Control) had normal feed and water; Group 2 (Untreated) was induced with AKI and left untreated. Group 3 and 4 took 50mg/kg and 500mg/kg L-arginine respectively after AKI induction. Acute kidney injury was induced by intra-muscular injection of glycerol (50% solution, 8 ml/kg BW). Oral glucose tolerance test, insulin response test, serum creatinine test and adiponectin assay (ELISA) were carried out. Data was analysed using one way ANOVA and expressed as mean± standard error of mean (SEM) with p ≤ 0.05 considered as significant. L-arginine induced rapid insulin-like action which was effective after thirty minutes of oral glucose loading when compared the control group. Glucose uptake from the blood was also more effective and quicker in the L-arginine treated groups. Adiponectin was significantly expressed across the test groups when compared to the control group and there was insulin resistance in the untreated kidney injured rats 1 hour into the insulin response test. It may be concluded that L-arginine has a homeostatic influence on glucose handling in kidney-damaged rats possibly mediated by increased adiponectin expression.

Discovery of seneciobipyrrolidine derivatives for the amelioration of glucose homeostasis disorders through 4E-BP1/Akt/AMPK signaling activation

Modulating the glucose transport in skeletal muscle is a promising strategy for ameliorating glucose homeostasis disorders. However, the complicated mechanisms of glucose transport make it difficult to find compounds therapeutically relevant molecular mechanisms of action, while phenotypic screening is thought to be an alternative approach to mimic the cell state of interest. Here, we report (±)-seneciobipyrrolidine (1a) is first found to enhance glucose uptake in L6 myotubes through phenotype-based screening. Further SAR investigation led to the identfication of compound A27 (EC50 = 2.7 μM). Proteomiic analysis discloses the unique function mechanism of A27 through upregulating the level of the eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1), subsequently enhancing the Akt and AMPK phosphorylation, thereby promoting the glucose uptake. Chronic oral administration of A27 significantly lowers blood glucose and improves glucose tolerance in db/db mice. This work is new research on seneciobipyrrolidine derivatives, providing a promising avenue for ameliorating glucose homeostasis.

Identification and analysis of sugar transporters capable of co-transporting glucose and xylose simultaneously.

Simultaneous co-fermentation of glucose and xylose is a key desired trait of engineered Saccharomyces cerevisiae for efficient and rapid production of biofuels and chemicals. However, glucose strongly inhibits xylose transport by endogenous hexose transporters of S. cerevisiae. We identified structurally distant sugar transporters (Lipomyces starkeyi LST1_205437 and Arabidopsis thaliana AtSWEET7) capable of co-transporting glucose and xylose from previously unexplored oleaginous yeasts and plants. Kinetic analysis showed that LST1_205437 had lenient glucose inhibition on xylose transport and AtSWEET7 transported glucose and xylose simultaneously with no inhibition. Modelling studies of LST1_205437 revealed that Ala335 residue at sugar binding site can accommodates both glucose and xylose. Docking studies with AtSWEET7 revealed that Trp59, Trp183, Asn145, and Asn179 residues stabilized the interactions with sugars, allowing both xylose and glucose to be co-transported. In addition, we altered sugar preference of LST1_205437 by single amino acid mutation at Asn365. Our findings provide a new mechanistic insight on glucose and xylose transport mechanism of sugar transporters and the identified sugar transporters can be employed to develop engineered yeast strains for producing cellulosic biofuels and chemicals.

A novel phenolic formulation for treating hepatic and peripheral insulin resistance by regulating GLUT4-mediated glucose uptake

Chronic insulin resistance suppresses muscle and liver response to insulin, which is partially due to impaired vesicle trafficking. We report here that a formula consisting of resveratrol, ferulic acid and epigallocatechin-3-O-gallate is more effective in ameliorating muscle and hepatic insulin resistance than the anti-diabetic drugs, metformin and AICAR. The formula enhanced glucose transporter-4 (GLUT4) translocation to the plasma membrane in the insulin-resistant muscle cells by regulating both insulin-independent (calcium and AMPK) and insulin-dependent (PI3K) signaling molecules. Particularly, it regulated the subcellular location of GLUT4 through endosomes to increase glucose uptake under insulin-resistant condition. Meanwhile, this phytochemicals combination increased glycogen synthesis and decreased glucose production in the insulin-resistant liver cells. On the other hand, this formula also showed anti-diabetic potential by the reduction of lipid content in the myotubes, hepatocytes, and adipocytes. This study demonstrated that the three phenolic compounds in the formula could work in distinct mechanisms and enhance both insulin-dependent and independent vesicles trafficking and glucose transport mechanisms to improve carbohydrate and lipid metabolism.

A Review of Microvascular Complications

Complications of Diabetes mellitus include chronic damage, dysfunction and disappointment of various organs mainly affecting the eyes, kidneys, heart and blood vessels. Various minerals and vitamins acts as cofactors in regulation of insulin secretion and action ,among which magnesium dramas a key role. Magnesium is an essential mineral and plays a major role in carbohydrate metabolism. It acts as a co-factor in glucose transport mechanism and for various intracellular enzymes involved in carbohydrate oxidation. Deficiency of magnesium results in increase in insulin resistance and decrease in glucose uptake of the cells in the body. Serum magnesium levels in healthy individuals are constant, but 25 to 39% people with Type 2DM have low levels of magnesium. Hypomagnesemia has been found to have deleterious effect on glucose homeostasis and insulin sensitivity in Type 2DM. Low levels of magnesium have also been attributed to the progression and development of micro and macrovascular difficulties in Type 2DM.

Lipid-Induced Mechanisms of Metabolic Syndrome.

Metabolic syndrome (MetS) has a worldwide tendency to increase and depends on many components, which explains the complexity of diagnosis, approaches to the prevention, and treatment of this pathology. Insulin resistance (IR) is the crucial cause of the MetS pathogenesis, which develops against the background of abdominal obesity. In light of recent evidence, it has been shown that lipids, especially fatty acids (FAs), are important signaling molecules that regulate the signaling pathways of insulin and inflammatory mediators. On the one hand, the lack of n-3 polyunsaturated fatty acids (PUFAs) in the body leads to impaired molecular mechanisms of glucose transport, the formation of unresolved inflammation. On the other hand, excessive formation of free fatty acids (FFAs) underlies the development of oxidative stress and mitochondrial dysfunction in MetS. Understanding the molecular mechanisms of the participation of FAs and their metabolites in the pathogenesis of MetS will contribute to the development of new diagnostic methods and targeted therapy for this disease. The purpose of this review is to highlight recent advances in the study of the effect of fatty acids as modulators of insulin response and inflammatory process in the pathogenesis and treatment for MetS.

Hypoglycemic effect of soluble polysaccharide and catechins from green tea on inhibiting intestinal transport of glucose.

Water soluble polysaccharide derived from green tea (WSP) is produced as byproducts when catechins were extracted from green tea. Although inhibitory effect of green tea catechins on the glucose transport in small intestine has been studied, the hypoglycemic efficacy of the WSP or its combinational effect has not been studied. In order to investigate hypoglycemic efficacy of the WSP or its combinational effect with green tea extract (GTE), co-consumption of GTE and WSP with wheat starch was investigated using in vitro digestion coupled with Caco-2 cells. The mechanism of the intestinal glucose transport was elucidated throughout the gene expression of the intestinal glucose transporters, which included sodium dependent glucose transporter (SGLT1) and glucose transporter 2 (GLUT2), using quantitative real-time polymerase chain reaction (qRT-PCR). The co-digestion of wheat starch with GTE during the small intestinal phase was the most rapidly digested into reducing sugar (73.96 g L-1 ) compared to itself (48.44 g L-1 ), WSP (60.35 g L-1 ), and GTE + WSP (61.81 g L-1 ). Intestinal glucose transport was 11.82, 7.59, 4.49, and 2.40% for wheat starch, wheat starch with GTE, WSP, and GTE + WSP, respectively. The highest decreased expression pattern in SGLT1 was observed when cells treated with wheat starch + GTE + WSP (0.66-fold) compared to GTE or WSP treatment. The results suggested that co-consumption of green tea derived products with wheat starch could delay the intestinal absorption of glucose. Results from the current study suggested that GTE and WSP could be the useful supplements of dietary therapy for hyperglycemia to delay glucose absorption. © 2020 Society of Chemical Industry.

Does hyperglycemia downregulate glucose transporters in the brain?

Diabetes is a metabolic condition associated with hyperglycemia manifested by the elevation of blood glucose levels occurring when the pancreas decreases or stops the production of insulin, in case of insulin resistance or both. The current literature supports that insulin resistance may be responsible for the memory decline associated with diabetes. Glucose transporters (GLUTs) are a family of proteins involved in glucose transport across biological membranes. GLUT-1 and GLUT-3 are involved in glucose delivery to the brain. Evidence suggests that both transporters are downregulated in chronic peripheral hyperglycemia. Here we show the mechanisms of glucose transport and its influence on cognitive function, including a hypothesis of how peripheral hyperglycemia related genes network interactions may lead to glucose transporters downregulation and its possible consequences.

Effect of chromium citrate on the mechanism of glucose transport and insulin resistance in Buffalo rat liver cells.

OBJECTIVE:Our published literature indicated that chromium citrate could regulate the glycemic index in alloxaninduced diabetic mice. The present study investigated the mechanism of chromium citrate in insulin resistance (IR) buffalo rat liver (BRL) cells.MATERIALS And METHODS:Chromium citrate was synthesized in our laboratory. BRL cells were purchased from the Chinese Academy of Sciences Cell Bank. The glucose transport and IR affected by chromium citrate in BRL cells were examined. The Thiazolyl Blue Tetrazolium Bromide (MTT) and glucose assay experiments were measured by microplate ELISA reader. The protein kinase B (Akt), glucose transporter-4 (Glut4), and phosphor-AMP-activated protein kinase β1 levels were tested by Western blot, and the mRNA expression of glucose transport proteins (Akt2, Glut4, and AMPactivated protein kinase α2 (AMPKα2)) and insulin sensitivity proteins (insulin receptor substrate1 (IRS-1), phosphatidylinositol 3 kinase (PI3K), and peroxisome proliferator-activated receptor γ (PPARγ)) was measured by reverse transcription–polymerase chain reaction.RESULTS:The results indicated that the glucose absorption level of chromium citrate groups was higher than model group significantly. It demonstrated that chromium citrate could significantly improve glucose absorption in IR BRL cells. The Akt, Glut4, and phosphor-AMPKβ1 levels in chromium citrate groups (at doses of 0.4, 0.2, and 0.1 μg Cr/mL) were markedly improved when compared with the other experiment groups, and chromium citrate could more effectively increase the Akt level than chromium trichloride. In addition, the mRNA expression of Akt2, Glut4, and AMPKα2 in chromium citrate groups was significantly improved when contrasted with model group.CONCLUSION:The consequences illustrated that chromium citrate can affect the IR BRL cells' ameliorating glucose transport and IR.

Positive correlation of psoriasis vulgaris severity and HOMA-IR

Background: Psoriasis vulgaris is a chronic inflammatory skin disease that its aetiology is still not completely known. A chronic inflammation in psoriasis can cause organ dysfunctions. Elevation of proinflammatory cytokines gives rise to insulin resistance by inhibiting insulin and glucose transport mechanism signals. Insulin resistance is the underlying pathogenesis of metabolic syndrome.Objective: This study aimed to undestand any correlation in the severity of psoriasis vulgaris with HOMA-IR.Methods: A cross sectional research involving 35 subjects with psoriasis vulgaris and 15 subjects without who met the selection criteria. HOMA-IR is a formula used to measure insulin resistance which calculates the fasting insulin value in μU/ml x fasting glucose in mg/DL/405 taken from the blood veins of subjects. PASI score was used to determine psoriasis vulgaris severity.Results: This study shows that the HOMA-IR median value was higher in psoriasis subject than the subjects without psoriasis (p&lt;0.05). The correlaton analysis shows a moderate positive correlation between psoriasis vulgaris severity and HOMA-IR (r= 0.427; p&lt;0.05). The prevalence ratio was 8.57, which means psoriasis vulgaris subjects were 8.57 times more likely to have HOMA-IR compared to those without psoriasis vulgaris (p&lt;0.05; 95%CI: 1.26-58.1).Conclusion: This study concludes that there is a moderate positive correlation between severity of psoriasis vulgaris and HOMA-IR values.