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To analyze the impact and distribution of blood groups in different ethnicities and the extent of susceptibility to infection with COVID-19 in Makkah, Saudi Arabia.A retrospective study was performed on 4,609 COVID-19 patients from five ethnic groups to assess the impact and distribution of different blood types and susceptibility to COVID-19 infection. The study was carried out between November 2020 and June 2021 in the College of Medicine, Umm Al-Qura University in collaboration with the General Directorate of Health Affairs, Makkah, Saudi Arabia.Blood group (A, B, and O) distributions in 2,617 COVID-19 patients with local control populations was done. Our study found that in both Saudi and non-Saudi populations, blood groups O and A were associated with higher infection rates, whereas blood group AB was associated with lower infection rates (We emphasize that COVID-19 infection is not proportional among ethnically related blood groups. Notably, RhD-negative protect against COVID-19, whereas A and O blood types are more susceptible. Thus, when assessing COVID-19 prognosis and vaccination priority, blood groups A and O are critical.

Purpose: To determine the antidiabetic effect of methanol extract of Plectranthus lanuginosus leaves in streptozotocin-induced hyperglycemic (HGD) rats. Methods: P. lanuginosus leaves were collected from Saad Medhas, Al Baha, Kingdom of Saudi Arabia. After defatting with n-hexane, they were extracted in vacuo at 40 oC with 75 % methanol. Streptozotocin (50 mgkg−1, i.p.) was used to induce hyperglycemia (diabetes) in the rats. The HGD rats received either standard drug (glibenclamide, 10 mgkg−1, p.o.) or Plectranthus lanuginosus leaf methanol leaf extract (PLLM) at doses of 200 and 400 mgkg−1/day, p.o. for 21 consecutive days. Blood samples were taken from the rat tails 2 h after dosing, and at 7-day intervals (i.e., 0, 7th, 14th and 21st days). The blood samples were used for measurement of fasting blood glucose (FBS), using a glucometer. On the 21st day, the rats were sacrificed via cardiac puncture. The activities of liver marker enzymes (SGPT and SGOT), and serum lipid profile (cholesterol, triglycerides, HDL and LDL) were determined using a hemolyzer. Results: Streptozotocin treatment produced significant hyperglycemia in the rats (348.9 ± 5.6) when compared to control (79.2 ± 1.3). However, PLLM (200 and 400 mg kg−1) produced significant and dose-dependent anti-diabetic (166.4 ± 5.6 and 123.86 ± 6.8 respectively) and antihyperlipidemic effects in HGD rats, at levels similar to those produced by the standard drug, glibenclamide (120.6 ± 6.4). Conclusion: P. lanuginosus leaf extract possesses pronounced anti-diabetic and anti-hyperlipidemic properties which may be due to the presence of phenolic and flavonoid constituents in the plant. Therefore, the plant extract can be further developed for the management of diabetes

Background: Hemodialysis (HD) patients with secondary Hyperparathyroidism (s-HPT) are exposed to increased inflammation and oxidative stress. In HD patients, oxidized albumin is a reliable marker of oxidative stress and its clinical significance has been rarely studied. Objective: The objective of this study was to evaluate Cys34 Human Serum Albumin (HSA) as oxidative stress biomarker in HD patients with s-HPT and its relationship with inflammation on bone turnover markers during oral calcitriol supplementation for vitamin D. Patients and Methods: Fifteen stable hemodialysis patients with s-HPT (mean age 48.67±8.15, 11 males and 4 females) were used in the experiment to receive calcitriol treatment for 16 weeks (0.25mcg or 0.5 mcg once a day according to serum level of Ca and P for each). The changes in the serum biochemical parameters (Ca, P, ALP, and iPTH), inflammatory markers (CRP and IL-6 levels) and serum oxidative stress condition (SOD, IS and albumin ratio HNA/HMA) were evaluated before and at 8 and 16 weeks of calcitriol treatment. The correlations between those factors were studied. Results: All patients responded to oral calcitriol therapy, with a significant decrease in the serum iPTH. The results showed that calcitriol could effectively suppress iPTH secretion with a significant elevation of serum Ca and P but ALP remained unchanged during the study. It can also effectively reduce the inflammatory markers (CRP and IL-6), while increasing the oxidative markers (SOD and IS). Oxidative albumin ratio HNA/HMA showed a significant (p=0.001) reduction after 16 weeks of calcitriol treatment and the redox state of HSA showed a positive prediction for hyperparathyroidism and for inflammation. Conclusion: The redox state of HSA could be used as a predictor for monitoring hyperparathyroidism and inflammation during calcitriol treatment by retarding albumin oxidation in HD patients with secondary hyperparathyroidism.

Purpose: Chronic hepatitis C has infected approximately 170 million people worldwide. The novel direct-acting antivirals have proven their clinical efficacy to treat hepatitis C infection but still very expensive and beyond the financial range of most infected patients in low income and even resource replete nations. This study was conducted to establish an in vitro stable human hepatoma 7 (Huh-7) cell culture system with consistent expression of the non-structural 5B (NS5B) protein of hepatitis C virus (HCV) 1a genotype and to explore inhibitory effects of sequence-specific short interference RNA (siRNA) targeting NS5B in stable cell clones, and against viral replication in serum-inoculated Huh-7 cells. Materials and Methods: In vitro stable Huh-7 cells with persistent expression of NS5B protein was produced under gentamycin (G418) selection. siRNAs inhibitory effects were determined by analysing NS5B expression at mRNA and protein level through reverse transcription-polymerase chain reaction (PCR), quantitative real-time PCR, and Western blot, respectively. Statistical significance of data (NS5B gene suppression) was performed using SPSS software (version 16.0, SPSS Inc.). Results: siRNAs directed against NS5B gene significantly decreased NS5B expression at mRNA and protein levels in stable Huh-7 cells, and a vivid decrease in viral replication was also exhibited in serum-infected Huh-7 cells. Conclusions: Stable Huh-7 cells persistently expressing NS5B protein should be helpful for molecular pathogenesis of HCV infection and development of anti-HCV drug screening assays. The siRNA was effective against NS5B and could be considered as an adjuvant therapy along with other promising anti-HCV regimens.

Obesity is a major health problem tremendously increasing worldwide, obesity has been accompanied by a state of metabolic dysregulation, characterized by insulin resistance and may be associated with many comorbidities such as metabolic syndrome, type 2 diabetes and cardiovascular complications. Lately a great attention has been gained toward the association of obesity with certain cancers. Numerous studies and meta-analysis reported that, obesity is associated with increased risk of esophageal adenocarcinoma, postmenopausal breast cancer, and endometrial, renal, pancreatic, prostate and colorectal cancers. In spite of, the evidence of such association that link obesity with risk and recurrence or death from cancer, however the linking mechanisms has not been yet fully explained. Obesity may promote cancer by: 1) alteration of adipocytokines: Leptin, adiponectin, resistin and visfatin with promotion of angiogenesis and interactions with other mediators and cytokines. 2) Hypoxia and angiogenesis due to expansion of adipose tissue with release of certain mediators that stimulate angiogenesis. 3) Metaflammation state of low grade and chronic inflammation that merely stimulate release of cytokines as (TNFα) and (IL-6) and the activation of pro-inflammatory signaling. 4) Insulin resistance with hyperinsulinemia and increased levels of insulin and growth factors as IGFs and IGF binding proteins. 5) Increased levels of sex steroids, including estradiol and Dehydroepiandrosterone (DHEA) particularly in cases of endometrial and postmenopausal breast cancers. 6) oxidative stress and reduction of antioxidants with possibility of oxidative damage or mutation of DNA. 7) epigenetic mechanisms, including DNA methylation , histones and chromatin remodeling factors . In fact, it remains unclear how the convergence of these mechanisms may drive obesity-associated cancer, considering the complex and multi-factorial characterization of cancer as well as the variation of genetics background of obese subjects. Prospective studies is worth pursuing especially towards therapeutic implications to prevent or treat obesity- associated cancer. Our aim is providing updated and comprehensive review about postulated and prospective links and molecular mechanisms between obesity and cancer, focusing upon mechanistic mediators that may drive obesity- associated cancers and may be targeted molecules for prospectives therapies. You can submit your Manuscripts at: https://symbiosisonlinepublishing.com/submitManuscript.php

Chronic hepatitis C has infected approximately 170 million people worldwide. The novel direct-acting antivirals have proven their clinical efficacy to treat hepatitis C infection but still very expensive and beyond the financial range of most infected patients in low income and even resource replete nations. This study was conducted to establish an in vitro stable human hepatoma 7 (Huh-7) cell culture system with consistent expression of the non-structural 5B (NS5B) protein of hepatitis C virus (HCV) 1a genotype and to explore inhibitory effects of sequence-specific short interference RNA (siRNA) targeting NS5B in stable cell clones, and against viral replication in serum-inoculated Huh-7 cells.In vitro stable Huh-7 cells with persistent expression of NS5B protein was produced under gentamycin (G418) selection. siRNAs inhibitory effects were determined by analysing NS5B expression at mRNA and protein level through reverse transcription-polymerase chain reaction (PCR), quantitative real-time PCR, and Western blot, respectively. Statistical significance of data (NS5B gene suppression) was performed using SPSS software (version 16.0, SPSS Inc.).siRNAs directed against NS5B gene significantly decreased NS5B expression at mRNA and protein levels in stable Huh-7 cells, and a vivid decrease in viral replication was also exhibited in serum-infected Huh-7 cells.Stable Huh-7 cells persistently expressing NS5B protein should be helpful for molecular pathogenesis of HCV infection and development of anti-HCV drug screening assays. The siRNA was effective against NS5B and could be considered as an adjuvant therapy along with other promising anti-HCV regimens.

1Department of Biochemistry, Faculty of Medicine, Umm Al-Qura University, Makkah, Kingdom of Saudi Arabia. 2Oncology Diagnostic Unit, Faculty of Medicine, Ain Shams University, Cairo, Egypt. 3King Faisal Hospitals, Shesha, Makkah, Kingdom of Saudi Arabia. 4Medical Genetics department, Faculty of Medicine, Umm Al-Qura University, Makkah, Kingdom of Saudi Arabia. 5Division of Human Genetics and Genome Research, Department of Molecular Genetics and Enzymology, National Research Centre, 33Bohouth St. Dokki, Giza, Egypt.

Doxorubicin is a commonly used anticancer agent, which may cause cardiac toxicity. The present study designed to evaluate Phoenix dactylofera (dates) in doxorubicin (DXR) induced cardiac toxicity and cardiac remodeling in Wistar albino rats. The experimental rats procured, acclimatized and finally divided into five groups (n = 6). Group I served as normal controls, group II served as disease controls and groups 3, 4 & 5 served as therapeutic groups (Phoenix dactylofera 5%, 10%, and 15% respectively). Cardiac remodeling and toxicity in the rats were induced by administration of DXR (1.25 mg/kg i.p. in 16 divided doses/month). At the end of protocol, effect of Phoenix dactylofera on cardiac remodeling was evaluated by measuring parameters like haemodynamics, heart weight, anatomy, Troponin T, creatine phosphokinase (CPK), creatine phosphokinase-MB (CPK-MB), Lactate dehydrogenase (LDH), serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), calcium ion Ca2+, sodium ion Na+, potassium ion K+, intracellular enzymes like Malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT). The disease control groups showed significantly elevated (p dactylofera significantly (p 2+, Na+, K+ levels to a normal value. Further, the histological studies of the cardiac tissues demonstrated that the normal architecture of the cardiac cells was restored in the animals fed with dietary Phoenix dactylofera as compared to disease controls. The findings show that the administration of Phoenix dactylofera has the potential to prevent the toxicity induced by doxorubicin in the experimental rats.

Background: Oxidative stress has been closely linked to the incidence of diabetic complications. Therefore, the aim of this research article was to study hyperglycemia and abnormal lipid profile in diabetic patient type 2 and its correlation with oxidative stress development as measured by 8-iso-PGF2α and 8-OHdG. Methods: Fifty (50) patients confirmed type 2 diabetes mellitus and eighty (80) non-diabetic control individuals were included in this study. All individuals were tested for blood glucose, lipid profile, 8-iso-PGF2α and 8-OHdG HdG. Results: The age of diabetic patients was observed to be ≥40 yrs in 96% and diabetes was frequently detected in female than in male patients (76% vs. 24%, p < 0.0001). Mean serum lipids were elevated in diabetic patients compared with control individuals (p < 0.0001) except in HDL-C, a significant decrease was recorded (p = 0.04). Serum 8-iso-PGF2α and 8-OHdG were elevated significantly in diabetic patients compared with non-diabetic control and a significant correlation was recorded between them (r = 0.6, p < 0.0001). 8-iso-PGF2α was associated with Age (r = 0.394, p < 0.0001), FBG (0.553, p < 0.0001), LDL-C (r = 0.2, p = 0.023), TG (r = 0.176, p = 0.045) and TC (r = 0.2, p = 0.02). Also, 8-OHdG was associated with age (r = 0.558, p < 0.0001), FBG (r = 0.67, p < 0.0001), LDL-C (r = 0.28, p = 0.001), TG (r = 0.358, p < 0.0001) and TC (r = 0.33, p < 0.0001). Age, FBG, HbA1c, LDL-C, TG and TC showed a significant linear regression with 8-iso-PGF2α and 8-OHdG recording its role as significant predictors for the elevation of 8-iso-PGF2α and 8-OHdG. Therefore, hyperglycemia with oxidative stress development may play a role for dyslipidemia and diabetic complications. Conclusion: Diabetic patient’s type 2 has a higher rate of abnormal serum lipids and correlates significantly with lipid peroxidation and oxidized DNA bases as measured by 8-iso-PGF2α and 8-OHdG. Therefore, 8-iso-PGF2α and 8-OHdG could be used as oxidative biomarkers for evaluating diabetic patients with early prediction of its complications and cancer development.

OBJECTIVE To explore inhibitory effects of genome-specific, chemically synthesized siRNAs (small interference RNA) against NS3 gene of hepatitis C virus (HCV) 1a genotype in stable Huh-7 (human hepatoma) cells as well as against viral replication in serum-inoculated Huh-7 cells. METHODS Stable Huh-7 cells persistently expressing NS3 gene were produced under antibiotic gentamycin (G418) selection. The cell clones resistant to 1000 μg antibiotic concentration (G418) were picked as stable cell clones. The NS3 gene expression in stable cell clone was confirmed by RT-PCR and Western blotting. siRNA cell cytotoxicity was determined by MTT cell proliferation assay. Stable cell lines were transfected with sequence specific siRNAs and their inhibitory effects were determined by RT-PCR, real-time PCR and Western blotting. The viral replication inhibition by siRNAs in serum inoculated Huh-7 cells was determined by real-time PCR. RESULTS RT-PCR and Western blot analysis confirmed NS3 gene and protein expression in stable cell lines on day 10, 20 and 30 post transfection. MTT cell proliferation assay revealed that at most concentrated dose tested (50 nmol/L), siRNA had no cytotoxic effects on Huh-7 cells and cell proliferation remained unaffected. As demonstrated by the siRNA time-dependent inhibitory analysis, siRNA NS3-is44 showed maximum inhibition of NS3 gene in stable Huh-7 cell clones at 24 (80%, P = 0.013) and 48 h (75%, P = 0.002) post transfection. The impact of siRNAs on virus replication in serum inoculated Huh-7 cells also demonstrated significant decrease in viral copy number, where siRNA NS3-is44 exhibited 70% (P

This study deals with the detection of serum p53 antigen concentration by enzyme-linked immunosorbent assay as a marker for TP53 gene mutation in gastric cancer patients, correlating it with p53 protein expression detected by immunostaining. The serum concentration of p53 antigen ranged from 0.28 ng/mL to 0.59 ng/mL [average 0.40 ± 0.08 ng/mL, (p

Background Helicobacter pylori (H. pylori) infection is reported to be associated with various extragastrointestinal conditions such as insulin resistance, diabetes mellitus and metabolic syndrome. H. pylori infection and type 2 diabetes mellitus (T2DM) are associated with oxidative stress, this cross-relation between H. pylori induced infection in T2DM and oxidative damage is still debated. Thus, the question arises whether an increase in the serum level of 8-OHdG and Ox-LDL will occurs in patients with T2DM infected H. pylori; this will be through determination and compare frequency of H. pylori infection in T2DM and non-diabetic patients. Methods 100 patients presented with history of epigastric discomfort for more than 1 month; 50 patients with T2DM and 50 non-diabetics. Anti-H. pylori IgG using ELISA, fasting and postprandial glucose level, glycated hemoglobin (HbA1c) and body mass index (BMI) was calculated. Serum 8-OHdG and Ox-LDL was measured using ELISA for the 100 patients and 50 control subject. Results Rates of H. pylori infection of T2DM and non-diabetic were 66 and 58 %, respectively, (p = 0.001). H. pylori IgG antibody was not correlated with HbA1c either in T2DM (p = 0.06) or non-diabetic (p = 0.25). Serum 8-OHdG level in T2DM with positive H. pylori infection showed a significant difference compared to non-diabetics with positive H. pylori infection (p = 0.001) and higher than that in T2DM with negative H. pylori. A correlation between 8-OHdG concentration and HbA1c in T2DM patients infected with H. pylori was observed (r = 0.39, p = 0.02). Serum Ox-LDL level in T2DM with positive H. pylori infection showed a significant difference compared to diabetics with both negative H. pylori infection and in non-diabetics with positive H. pylori infection (p = 0.001). Conclusions Increased levels of oxidative DNA damage (8-OHdG) and Ox-LDL suggest the mechanistic link between H. pylori infection combined with diabetes and increased generation of ROS and could play as an important image for high risk to atherosclerosis.

The rate of glucose phosphorylation in hepatocytes is determined by the subcellular location of glucokinase and by its association with its regulatory protein (GKRP) in the nucleus. Elevated glucose concentrations and precursors of fructose 1-phosphate (e.g., sorbitol) cause dissociation of glucokinase from GKRP and translocation to the cytoplasm. In this study, we investigated the counter-regulation of substrate-induced translocation by AICAR (5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside), which is metabolized by hepatocytes to an AMP analog, and causes activation of AMP-activated protein kinase (AMPK) and depletion of ATP. During incubation of hepatocytes with 25 mM glucose, AICAR concentrations below 200 μM activated AMPK without depleting ATP and inhibited glucose phosphorylation and glucokinase translocation with half-maximal effect at 100–140 μM. Glucose phosphorylation and glucokinase translocation correlated inversely with AMPK activity. AICAR also counteracted translocation induced by a glucokinase activator and partially counteracted translocation by sorbitol. However, AICAR did not block the reversal of translocation (from cytoplasm to nucleus) after substrate withdrawal. Inhibition of glucose-induced translocation by AICAR was greater than inhibition by glucagon and was associated with phosphorylation of both GKRP and the cytoplasmic glucokinase binding protein, 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFK2) on ser-32. Expression of a kinase-active PFK2 variant lacking ser-32 partially reversed the inhibition of translocation by AICAR. Phosphorylation of GKRP by AMPK partially counteracted its inhibitory effect on glucokinase activity, suggesting altered interaction of glucokinase and GKRP. In summary, mechanisms downstream of AMPK activation, involving phosphorylation of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase and GKRP are involved in the ATP-independent inhibition of glucose-induced glucokinase translocation by AICAR in hepatocytes.

The role of glucose 6-P (glucose 6-phosphate) in regulating the activation state of glycogen synthase and its translocation is well documented. In the present study, we investigated the effects of glucose 6-P on the activation state and compartmentation of phosphorylase in hepatocytes. Glucose 6-P levels were modulated in hepatocytes by glucokinase overexpression or inhibition with 5-thioglucose and the effects of AMP were tested using AICAR (5-aminoimidazole-4-carboxamide 1-β-d-ribofuranoside), which is metabolized to an AMP analogue. Inhibition of glucokinase partially counteracted the effect of glucose both on the inactivation of phosphorylase and on the translocation of phosphorylase a from a soluble to a particulate fraction. The increase in glucose 6-P caused by glucokinase overexpression caused translocation of phosphorylase a to the pellet and had additive effects with glucose on inactivation of phosphorylase. It decreased the glucose concentration that caused half-maximal inactivation from 20 to 11 mM, indicating that it acts synergistically with glucose. AICAR activated phosphorylase and counteracted the effect of glucose 6-P on phosphorylase inactivation. However, it did not counteract translocation of phosphorylase by glucose 6-P. Glucose 6-P and AICAR had opposite effects on the activation state of glycogen synthase, but they had additive effects on translocation of the enzyme to the pellet. There was a direct correlation between the translocation of phosphorylase a and of glycogen synthase to the pellet, suggesting that these enzymes translocate in tandem. In conclusion, glucose 6-P causes both translocation of phosphorylase and inactivation, indicating a more complex role in the regulation of glycogen metabolism than can be explained from regulation of glycogen synthase alone.

Introduction: Gastric cancer (GC) remains a major public health problem worldwide being the third commonest cause of cancer death worldwide. Many recent studies focus on the immunohistochemical evaluation of Bcl-2 expression and its serum expression and its prognostic significance in gastric cancer each one separately. We conducted our study to determine the correlation between serum Bcl-2 antigen and gastric carcinoma, to investigate whether serum Bcl-2 concentrations can be used as marker for immunohistochemical determination of Bcl-2 alterations in gastric cancer patients and examine the association between its expression and other clinicopathological parameters. Methods: Our study conducted in Forty-five consecutive patients with gastric cancer underwent gastrectomy in Mansoura Gastroenterology Center. ELISA was used for the estimation of serum Bcl-2 levels in patients with different stages of gastric cancer. Immunohistochemical localization of Bcl-2 antigen was performed on formalinfixed, paraffin-embedded tissue block; Bcl-2 expression was detected from mild to moderate apoptotic index (AI). Results: Positive serum Bcl-2 expression was found in 13/45 patients (28.9%). Bcl-2 protein was immunohistochemically localized in the cytoplasm of 45% (18/40) of gastric cancer patients. Total apoptosis positivity in Bcl2 detected immunohistochemicaly was detected in 45% (18/ 40) of cases; while total apoptosis positivity in serum expression of Bcl-2 was detected in 28.9% (13/ 45). Conclusion: our current study demonstrated that the formation and growth of cancer is a complex process that requires further research in correlation with the results assessed between serum and immunohistochemical expression of Bcl-2 and with its role in the process of apoptosis.

Glucokinase has a very high flux control coefficient (greater than unity) on glycogen synthesis from glucose in hepatocytes (Agius et al., J. Biol. Chem. 271, 30479-30486, 1996). Hepatic glucokinase is inhibited by a 68-kDa glucokinase regulatory protein (GKRP) that is expressed in molar excess. To establish the relative control exerted by glucokinase and GKRP, we applied metabolic control analysis to determine the flux control coefficient of GKRP on glucose metabolism in hepatocytes. Adenovirus-mediated overexpression of GKRP (by up to 2-fold above endogenous levels) increased glucokinase binding and inhibited glucose phosphorylation, glycolysis, and glycogen synthesis over a wide range of concentrations of glucose and sorbitol. It decreased the affinity of glucokinase translocation for glucose and increased the control coefficient of glucokinase on glycogen synthesis. GKRP had a negative control coefficient of glycogen synthesis that is slightly greater than unity (-1.2) and a control coefficient on glycolysis of -0.5. The control coefficient of GKRP on glycogen synthesis decreased with increasing glucokinase overexpression (4-fold) at elevated glucose concentration (35 mM), which favors dissociation of glucokinase from GKRP, but not at 7.5 mM glucose. Under the latter conditions, glucokinase and GKRP have large and inverse control coefficients on glycogen synthesis, suggesting that a large component of the positive control coefficient of glucokinase is counterbalanced by the negative coefficient of GKRP. It is concluded that glucokinase and GKRP exert reciprocal control; therefore, mutations in GKRP affecting the expression or function of the protein may impact the phenotype even in the heterozygote state, similar to glucokinase mutations in maturity onset diabetes of the young type 2. Our results show that the mechanism comprising glucokinase and GKRP confers a markedly extended responsiveness and sensitivity to changes in glucose concentration on the hepatocyte.

Glucokinase is rapidly exported from the nucleus of hepatocytes in response to a rise in glucose or fructose 1-P. We demonstrate using confocal microscopy and quantitative imaging that in contrast to previous findings, the regulatory protein of glucokinase (GKRP) also translocates from the nucleus during substrate-induced translocation of glucokinase. However, the fractional decrease in nuclear GKRP is smaller than for glucokinase and is determined by the metabolic state and not by the distribution of glucokinase. Translocation of glucokinase and GKRP is not inhibited by leptomycin B, an inhibitor of exportin-1 function. These findings highlight the importance of quantitative imaging for determining nuclear export of proteins and suggest that GKRP may have a role in nuclear export or import of glucokinase.