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Insulin resistance - Top 30 Publications

Angiotensin receptor blockade improves cardiac mitochondrial activity in response to an acute glucose load in obese insulin resistant rats.

Hyperglycemia increases the risk of oxidant overproduction in the heart through activation of a multitude of pathways. Oxidation of mitochondrial enzymes may impair their function resulting in accumulation of intermediates and reverse electron transfer, contributing to mitochondrial dysfunction. Furthermore, the renin-angiotensin system (RAS) becomes inappropriately activated during metabolic syndrome, increasing oxidant production. To combat excess oxidant production, the transcription factor, nuclear factor erythriod-2- related factor 2 (Nrf2), induces expression of many antioxidant genes. We hypothesized that angiotensin II receptor type 1 (AT1) blockade improves mitochondrial function in response to an acute glucose load via upregulation of Nrf2. To address this hypothesis, an oral glucose challenge was performed in three groups prior to dissection (n = 5-8 animals/group/time point) of adult male rats: 1) Long Evans Tokushima Otsuka (LETO; lean strain-control), 2) insulin resistant, obese Otsuka Long Evans Tokushima Fatty (OLETF), and 3) OLETF + angiotensin receptor blocker (ARB; 10mg olmesartan/kg/d × 6 weeks). Hearts were collected at T0, T60, and T120 minutes post-glucose infusion. ARB increased Nrf2 binding 32% compared to OLETF at T60. Total superoxide dismutase (SOD) and catalase (CAT) activities were increased 45% and 66% respectively in ARB treated animals compared to OLETF. Mitochondrial enzyme activities of aconitase, complex I, and complex II increased by 135%, 33% and 66%, respectively in ARB compared to OLETF. These data demonstrate the protective effects of AT1 blockade on mitochondrial function during the manifestation of insulin resistance suggesting that the inappropriate activation of AT1 during insulin resistance may impair Nrf2 translocation and subsequent antioxidant activities and mitochondrial function.

Inverse association of marijuana use with nonalcoholic fatty liver disease among adults in the United States.

The impact of marijuana on nonalcoholic fatty liver disease (NAFLD) is largely unknown. We studied the association between marijuana and NAFLD utilizing cross-sectional data from the National Health and Nutrition Examination Survey (NHANES) from 2005-2014 and NHANES III (1988-1994).

High genetic risk scores for impaired insulin secretory capacity doubles the risk for type 2 diabetes in Asians and is exacerbated by Western-type diets.

Asians have among the highest incidence of type 2 diabetes (T2DM) in the world, partly due to low β-cell function, causing them to rapidly develop T2DM when insulin resistant. This study tested the hypothesis that genetic polymorphisms are responsible for the low β-cell function and that dietary factors interact with the genes to exacerbate their risk of T2DM.

N-acetylglucosamine: more than a silent partner in insulin resistance.

Pedersen et al. (Pedersen HK, Gudmundsdottir V, Nielsen HB, Hyotylainen T, Nielsen T, Jensen BA, Forslund K, Hildebrand F, Prifti E, Falony G, et al. 2016. Human gut microbes impact host serum metabolome and insulin sensitivity. Nature. 535: 376-381.) report that human serum levels of branched-chain amino acids (BCAA) and N-acetylglucosamine (GlcNAc) increase in proportion to insulin resistance. They focus on the microbiome and the contributing subset of microbe species, thereby demonstrating disease causality in mice. As either oral GlcNAc or BCAA in mice are known to increase insulin resistance and weight gain, we note that recently published molecular data argues for a cooperative interaction.

A Gender-Specific Association between Self-Reported Snoring and Hemoglobin A1c Levels in a General Population without Type 2 Diabetes Mellitus.

We explored whether a gender difference was evident in terms of the associations of snoring with hemoglobin A1c (HbA1c) and homeostatic model assessment-insulin resistance (HOMA-IR) levels in a healthy population without type 2 diabetes mellitus (DM).

Long-term feeding of high-fat plus high-fructose diet induces isolated impaired glucose tolerance and skeletal muscle insulin resistance in miniature pigs.

During the prediabetic development, the changes in β-cell function and tissue-specific insulin resistance have been described. However, there are conflicting views in insulin secretory capacity between early clinical observation and recent proposed mathematical model. On the basis of digestive and metabolic similarities with humans, swine have great potential as an animal model to investigate the progressive mechanisms of prediabetes. The aim of this study was to investigate the insulin secretory response and tissue-specific insulin resistance in a dietary-induced prediabetic porcine model.

Genetic Support for a Causal Role of Insulin Resistance on Circulating Branched-Chain Amino Acids and Inflammation.

Insulin resistance has deleterious effects on cardiometabolic disease. We used Mendelian randomization analyses to clarify the causal relationships of insulin resistance (IR) on circulating blood-based metabolites to shed light on potential mediators of the IR to cardiometabolic disease relationship.

Dicarbonyl Stress and Glyoxalase Enzymatic System Regulation in Human Skeletal Muscle.

Skeletal muscle insulin resistance is a hallmark of Type II Diabetes (T2DM) and may be exacerbated by protein modifications by methylglyoxal (MG), known as dicarbonyl stress. The glyoxalase enzyme system composed of glyoxalase 1/2 (GLO1/GLO2) is the natural defense against dicarbonyl stress, yet its protein expression, activity and regulation remain largely unexplored in skeletal muscle. Therefore, this study investigated dicarbonyl stress and the glyoxalase enzyme system in the skeletal muscle of subjects with T2DM (age: 56 ± 5 yrs; BMI: 32 ± 2 kg/m(2)) compared to lean healthy control subjects (LHC; age: 27 ± 1 yrs; BMI: 22 ± 1 kg/m(2)). Skeletal muscle biopsies obtained from the vastus lateralis at basal and insulin-stimulated states of the hyperinsulinemic (40 mU/m(2)/min) -euglycemic (5 mM) clamp were analyzed for proteins related to dicarbonyl stress and glyoxalase biology. At baseline, T2DM had increased carbonyl stress and lower GLO1 protein expression (-78.8%, p<0.05), which inversely correlated with BMI, percent body fat and HOMA-IR while positively correlating with clamp derived glucose disposal rates. T2DM also had lower NRF2 protein expression (-31.6%, p<0.05), which is a positive regulator of GLO1, while Keap1 protein expression, a negative regulator of GLO1, was elevated (207%, p<0.05). Additionally, insulin stimulation during the clamp had a differential effect on NRF2, Keap1 and MG-modified protein expression. These data suggest that dicarbonyl stress and the glyoxalase enzyme system are dysregulated in T2DM skeletal muscle and may underlie skeletal muscle insulin resistance. Whether these phenotypic differences contribute to the development of T2DM warrants further investigation.

The association between sex hormone-binding globulin and type 2 diabetes in Nigerian men.

Epidemiological studies have shown that sex hormone-binding globulin (SHBG) has a role in glucose homeostasis in both men and women. However, a prospective study on Japanese-American subjects concluded that SHBG was not a significant risk factor in either men or women, suggesting ethnic differences. We were not aware of any evaluation of SHBG in subjects of African ancestry.

Dietary Recommendations in Metabolic Vascular Syndrome.

Cardiovascular disease is the number one cause of death globally. Poor diet constitutes a key factor in the initiation and progression of cardiovascular disease and has become the leading risk factor for disability and death worldwide. Therefore, addressing suboptimal nutrition is of key prognostic relevance in primary and secondary prevention of metabolic vascular syndrome.Metabolic vascular syndrome is a multidimensional network of acquired cardiometabolic risk factors closely related to insulin resistance (IR) and concomitant hyperinsulinemia. IR, being the underlying cause of metabolic vascular syndrome and certain types of cancer, should attract the attention of every clinician. As changes in lipoprotein metabolism are one of the earliest indicators of metabolic dysfunction, a relevant biomarker for identifying individuals with IR is the TAG/HDL-C ratio.IR - and concomitant metabolic vascular risk - can be effectively treated by lifestyle intervention. If IR is present, dietary carbohydrate restriction has consistently been shown to be superior to dietary fat restriction in reversing metabolic dysfunction. The beneficial effects of carbohydrate restricted diets on metabolic vascular risk are independent of BMI - diet quality therefore confers patient benefit beyond weight reduction.The effect of single nutrients on isolated lipid surrogate markers such as LDL-C does not capture their global effect on metabolic vascular risk.Targeting IR with a low glycemic load, real food diet will reduce overall energy density and will improve all risk factors of metabolic vascular syndrome. In particular, replacing refined carbohydrates with healthy fats in the context of a Mediterranean style-, low carbohydrate and calorie-unrestricted dietary pattern has been shown to significantly reduce burden of metabolic vascular disease.

Anti-Diabetic Potential of the Leaves of Anisomeles malabarica in Streptozotocin Induced Diabetic Rats.

Diabetes mellitus is a pandemic metabolic disorder that is affecting a majority of populations in recent years. There is a requirement for new drugs that are safer and cheaper due to the side effects associated with the available medications.


We investigated concentrations and roles of insulin-like growth factor 1 (IGF-1) and its binding protein (IGF1BP-3), growth hormone (GH), insulin, and markers of insulin resistance and inflammation in acute myocardial infarction (AMI). We aimed to assess any possible association between serum GH/IGF-1 axis following AMI and short-term survival rates. A follow up study was performed in 2010. Study group consisted of 75 patients with Killip I and II class AMI. There were 30 control subjects. Blood samples were obtained within 24 hours of admission and analyzed for the aforementioned hormones. Patients were followed-up during 6 months for new cardiac events. Median GH was higher in AMI (0.96; range 0.6-2.4) than in controls (0.26; p<0.001). IGF-1 was significantly lower in AMI (123 vs. 132; p<0.05), and so was the IGF-1/GH ratio (p<0.001) and IGF1BP-3. Insulin was higher in study group, but without statistical significance. However, we found significant between-group differences in other markers of insulin resistance (HbA1c, glycemia, HOMA-IR) and inflammation. Simple linear correlation showed positive correlation between GH and C-reactive protein. All patients with new cardiac events had IGF-1 below median and lower left ventricular ejection fraction. In conclusion, IGF-1 may affect outcome of AMI. GH resistance might be a result of inflammatory/immune response and therefore it could be a useful prognostic marker.

Insulin secretory defect in familial partial lipodystrophy type 2 and successful long-term treatment with a glucagon-like peptide 1 receptor agonist.

Familial partial lipodystrophies are rare monogenic disorders that are often associated with diabetes. In such cases, it can be difficult to achieve glycaemic control.

An inverse association between serum resistin levels and n-3 polyunsaturated fatty acids intake was strongest in the SNP-420 G/G genotype in the Japanese cohort: The Toon Genome Study.

Resistin is secreted from monocytes/macrophages and is associated with insulin resistance, inflammation, and cardiovascular diseases. In the Japanese cohort, serum resistin is tightly associated with a single nucleotide polymorphism (SNP) at -420 (rs1862513) in the promoter region of the human resistin gene. However, interactions between SNP-420 and environmental factors remain to be elucidated. The aim of this study was to investigate the association between serum resistin levels and nutrient intake, and the effect of SNP-420 on this association.

Rituximab for the treatment of type B insulin resistance syndrome: a case report and review of the literature.

Type B insulin resistance syndrome is a rare disease characterized by refractory transient hyperglycaemia and severe insulin resistance associated with circulating anti-insulin receptor antibodies. A standardized treatment regimen for type B insulin resistance syndrome has yet to be established.

Women with polycystic ovary syndrome demonstrate worsening markers of cardiovascular risk over the short-term despite declining hyperandrogenaemia: Results of a longitudinal study with community controls.

To compare age-associated changes in cardiovascular risk markers in lean and obese reproductive-aged women with polycystic ovary syndrome (PCOS) with community controls DESIGN: Longitudinal study at an academic medical centre.

The relationship between serum vitamin D levels and cardiovascular risk factors among Icelandic children.

To determine the relationship between serum vitamin D levels and known cardiometabolic risk factors among healthy Icelandic children as well as study these connections independent of body mass index (BMI).

Associations Among Fatty Acids, Desaturase and Elongase, and Insulin Resistance in Children.

Fatty acid profiles and desaturase (SCD-16, SCD018, D5D, D6D) and elongase (ELOVL6) enzyme activity have been associated with adiposity and metabolic disease. While this has been studied in adults, few studies have included children. The objective of this study was to evaluate these markers in children and identify relationships with markers of metabolic health. It was hypothesized that these lipid markers would be correlated to adiposity and metabolic disease.

Antihypertensive effects of Tartary buckwheat flavonoids by improvement of vascular insulin sensitivity in spontaneously hypertensive rats.

Vascular insulin resistance and oxidative stress contribute to endothelial dysfunction and hypertension. The present study investigated whether chronic treatment with purified Tartary buckwheat flavonoids fraction (TBF) prevents the development of hypertension via improving vascular insulin sensitivity and reducing oxidative stress. Six-week-old male spontaneously hypertensive rats (SHRs) and their normotensive Wistar-Kyoto (WKY) control rats were subjected to different dosages of TBF for 8 weeks. Blood pressure, mesenteric arteriolar vasorelaxation, superoxide anion (O2(-)) generation, NAD(P)H oxidase activity, and insulin-stimulated Akt/endothelial nitric oxide synthase (eNOS) activation and nitric oxide (NO) production were determined. The SHRs had higher systolic blood pressure, systemic insulin resistance, and impaired vasodilator actions of insulin and the insulin signaling pathway in mesenteric arterioles when compared with the WKY rats. TBF treatment at a dosage of 100 mg kg(-1) day(-1) significantly reduced systolic blood pressure and increased vasodilator response to insulin in the SHRs. Additionally, TBF treatment significantly reduced phosphorylation of insulin receptor substrate 1 (IRS-1) at serine 307 and increased insulin-stimulated Akt/eNOS activation in the SHRs. Furthermore, TBF treatment reduced the overproduction of basal O2(-) in association with a reduction of NAD(P)H oxidase activity in mesenteric arterioles of the SHRs. Finally, quercetin was identified as the predominant active component of TBF in attenuating the development of hypertension with regard to reducing vascular oxidative stress, regulating the vascular insulin signaling pathway and restoring vasodilator response to insulin in the SHRs. In conclusion, TBF possesses protective effects against hypertension through attenuating vascular insulin resistance and oxidative stress.

Vitamin A Improves Hyperglycemia and Glucose-Intolerance through Regulation of Intracellular Signaling Pathways and Glycogen Synthesis in WNIN/GR-Ob Obese Rat Model.

Vitamin A and its metabolites modulate insulin resistance and regulate stearoyl-CoA desaturase 1 (SCD1), which are also known to affect insulin resistance. Here, we tested, whether vitamin A-mediated changes in insulin resistance markers are associated with SCD1 regulation or not. For this purpose, 30-week old male lean and glucose-intolerant obese rats of WNIN/GR-Ob strain were given either a stock or vitamin A-enriched diet, i.e. 2.6 mg or 129 mg vitamin A/kg diet, for 14 weeks. Compared to the stock diet, vitamin A-enriched diet feeding improved hyperglycemia and glucose-clearance rate in obese rats and no such changes were seen in lean rats receiving identical diets. These changes were corroborated with concomitant increase in circulatory insulin and glycogen levels of liver and muscle (whose insulin signaling pathway genes were up-regulated) in obese rats. Further, the observed increase in muscle glycogen content in these obese rats could be explained by increased levels of the active form of glycogen synthase, the key regulator of glycogen synthesis pathway, possibly inactivated through increased phosphorylation of its upstream inhibitor, glycogen synthase kinase. However, the unaltered hepatic SCD1 protein expression (despite decreased mRNA level) and increased muscle-SCD1 expression (both at gene and protein levels) suggest that vitamin A-mediated changes on glucose metabolism are not associated with SCD1 regulation. Chronic consumption of vitamin A-enriched diet improved hyperglycemia and glucose-intolerance, possibly, through the regulation of intracellular signaling and glycogen synthesis pathways of muscle and liver, but not associated with SCD1.

Meta-fibrosis links positive energy balance and mitochondrial metabolism to insulin resistance.

Obesity and insulin resistance often emerge from positive energy balance and generally are linked to low-grade inflammation. This low-grade inflammation has been called "meta-inflammation" because it is a consequence of the metabolic dysregulation that can accompany overnutrition. One means by which meta-inflammation is linked to insulin resistance is extracellular matrix expansion secondary to meta-inflammation, which we define here as "meta-fibrosis". The significance of meta-fibrosis is that it reflects a situation in which the extracellular matrix functions as a multi-level integrator of local (for example, mitochondrial reactive oxygen species production) and systemic (for example, inflammation) inputs that couple to cellular processes creating insulin resistance. While adipose tissue extracellular matrix remodeling has received considerable attention, it is becoming increasingly apparent that liver and skeletal muscle extracellular matrix remodeling also contributes to insulin resistance. In this review, we address recent advances in our understanding of energy balance, mitochondrial energetics, meta-inflammation, and meta-fibrosis in the development of insulin resistance.

CD19(+)CD24(hi)CD38(hi) regulatory B cells are associated with insulin resistance in type I Hashimoto's thyroiditis in Chinese females.

Hashimoto's thyroiditis (HT) is typically associated with insulin resistance. The aim of the present study was to investigate the role of regulatory B cells (Bregs) in insulin resistance in patients with HT. A total of 52 female patients with type I HT and 35 matched healthy volunteers were enrolled. Demographic and laboratorial data were collected. A 75 g oral glucose tolerance test was performed on each subject. Flow cytometry was performed to evaluate the levels of CD19(+)CD24(hi)CD38(hi) Bregs in peripheral blood. Patients with HT exhibited significantly higher postprandial insulin levels (P<0.01), but normal glucose levels. The level of CD19(+)CD24(hi)CD38(hi) Bregs in patients with HT decreased significantly (P=0.0002) compared with the controls. Pearson's linear correlation model revealed a significant, negative association between anti-thyroid peroxidase antibodies (TPOAb) and homeostasis model assessment of β cell (r=-0.313, P=0.014). The same correlation model revealed a significant, negative association between TPOAb and the disposition index (DI; r=-0.305, P=0.017), and between anti-thyroglobulin antibodies and DI (r=-0.321, P=0.013). Patients with a decreased ratio of CD19(+)CD24(hi)CD38(hi) Bregs to CD19(+) lymphocytes exhibited higher levels of total cholesterol and low-density lipoprotein cholesterol. A decrease in the ratio of CD19(+)CD24(hi)CD38(hi) Bregs to lymphocytes was a significant independent risk factor for hyperinsulinemia (odds ratio=1.372, P=0.035). A decrease in peripheral blood CD19(+)CD24(hi)CD38(hi) Bregs is associated with insulin resistance in HT patients, and was an independent risk factor for postprandial hyperinsulinemia. The present study provided a novel insight into the development of effective therapeutic strategies targeting immune mechanisms associated with HT.

1α,25-Dihydroxyvitamin D3 promotes bone formation by promoting nuclear exclusion of the FoxO1 transcription factor in diabetic mice.

1α,25-Dihydroxyvitamin D3 (1,25(OH)2D3) is the active form of vitamin D, which is responsible for reducing the risk for diabetes mellitus (DM), decreasing insulin resistance, and improving insulin secretion. Previous studies have shown that 1,25(OH)2D3 inhibited the activity of FoxO1, which has been implicated in the regulation of glucose metabolism. However, its function and mechanism of action in DM-induced energy disorders and also in bone development remains unclear. Here, using in vitro and in vivo approaches including osteoblast-specific, conditional FoxO1-knockout mice, we demonstrate that 1,25(OH)2D3 ameliorates abnormal osteoblast proliferation in DM-induced oxidative stress conditions, and rescues the impaired glucose and bone metabolism through FoxO1 nuclear exclusion resulted from the activation of PI3K/Akt signaling. Using Alizarin red staining, Alkaline phosphatase assay, Western blot and Real-time qPCR techniques, we found that 1,25(OH)2D3 promotes osteoblast differentiation and expression of osteogenic phenotypic markers (i.e. alkaline phosphatase (1), collagen 1 [COL-1], osteocalcin [OCN], and osteopontin [OPN]) in a high-glucose environment. Moreover, 1,25(OH)2D3 increased both total OCN secretion and levels of uncarboxylated OCN (GluOC) by phosphorylating FoxO1 and promoting its nuclear exclusion, indicated by Western blot and cell immunofluorescence analyses. Taken together, our findings confirm that FoxO1 is a key mediator involved in glucose homeostasis and indicate that 1,25(OH)2D3 improves glucose metabolism and bone development via regulation of PI3K/Akt/FoxO1/OCN pathway.

Ginsenoside Rg3 ameliorated HFD-induced hepatic steatosis through downregulation of STAT5-PPARγ.

Healthy expansion of adipose tissue maintains metabolic homeostasis by storing excess chemical energy in increased fat mass. The STAT5-PPAR gamma pathway reportedly regulates adipocyte differentiation, lipid metabolism and adipogenesis. Ginsenoside Rg3 is one of the diverse groups of steroidal saponins, the major active components of ginseng, which have demonstrated pharmacological properties. In this study, we evaluated the therapeutic effects of ginsenoside Rg3 under pathological conditions in vitro and in vivo We examined the effects of ginsenoside Rg3 on glucose level, insulin sensitivity and lipogenesis in high-fat diet-fed C57BL/6 mice. Ginsenoside Rg3 was also applied to the pre-adipocyte cell line 3T3-L1 to assess the impact on lipogenesis. Ginsenoside Rg3 reduced epididymal white adipose tissue (eWAT) size and hepatic steatosis, and the amount of triglycerides (TGs) in both eWAT and liver. Similar to the murine model, Rg3-treated 3T3-L1 cells showed a reduction in lipid accumulation and amount of total TGs. Ginsenoside Rg3 regulates the expression of PPAR gamma though STAT5 in vitro and in vivo According to our results, lipid metabolism-related genes were downregulated in the high-fat mice and 3T3-L1 cell line. Rg3 shows potential for the amelioration of obesity-induced pathology, acting though STAT5-PPAR gamma to facilitate the healthy functioning of adipose tissue. This is the first report of evidence that obesity-induced insulin resistance and lipotoxicity can be treated with ginsenoside Rg3, which acts though the STAT5-PPAR gamma pathway in vivo and in vitro.

Incretins in patients with rheumatoid arthritis.

The precise mechanism linking systemic inflammation with insulin resistance (IR) in rheumatoid arthritis (RA) remains elusive. In the present study, we determined whether the incretin-insulin axis and incretin effect are disrupted in patients with RA and if they are related to the IR found in these patients.

Depression in the Context of Medical Disorders: New Pharmacological Pathways Revisited.

The depressive state has been characterised as one of elevated inflammation, changed cardiovascular parameters and a deranged metabolic situation all of which holds promise for a better understanding and handling of treatment-resistance in affective disorders as well as for future developments in treatment algorithms. In this context several biomarkers are differentially regulated by antidepressant treatment and connected to metabolic, inflammatory, cardiovascular and apoptotic components of the pathophysiology, i.e. adiponectin, apolipoprotein-B, B-type natriuretic peptide, cortisol, CRP, cysteine, homocysteine, fibrinogen, adiponectin, BMI, glycated hemoglobin A1c, leptin, interferon-gamma, high-density lipoprotein, interleukin interleukin-1alpha, -1beta, -2, -4, -5, -6, -8, -10, -12, -13, -17, insulin-like growth factor-1, low-density lipoprotein, myeloperoxidase, osteoprotegerin, tumour necrosis factor alpha, troponins, triglycerides etc. In this context antidepressants exert different modulatory effects on the outcome, incidence and mortality concerning several severe disorders, i.e. cancer, diabetes, stroke, inflammation, stroke and cardiovascular risk. Vice versa different drugs used in the treatment of these disorders have a favourable effect in depressive states, e.g. statins, aspirine, NSAIDs, pioglitazone, celecoxib, peroxisome proliferator-activated receptor-gamma agonists and minocycline. In this review, actions of different antidepressant treatment strategies on cancer, stroke, diabetes and cardiovascular disorders are shown and the influence on the outcome of the disorders is differentially discussed. In conclusion a hypothetic model for the implication of actual findings in everyday clinical practice is proposed. In this context personalized treatment could be used to tailor treatment to specific individuals according to their clinical endophenotypes. Moreover a potential target for the development of novel intervention strategies might be used.

Polymorphisms in adrenergic receptor genes in Qinchuan cattle show associations with selected carcass traits.

The beta-adrenergic receptors coded by the ADRB1, ADRB2 and ADRB3 genes play important roles in mediating metabolic effects, especially lipolysis, insulin resistance and energy balance. This study investigated the expression levels of these three genes in different tissues of Qinchuan cattle by real-time polymerase chain reaction (RT-PCR). Expressed levels of RNA from the ADRB2 gene were generally much higher than for ADRB1 and ADRB3. ADRB1 and ADRB2 expression levels were highest in subcutaneous fat and lower in muscle, whereas ADRB3 expression was higher in muscle tissue. Eight single nucleotide polymorphisms (SNPs) were discovered in 503 Qinchuan cattle by DNA sequencing, containing three missense mutations (g.1148G>C in ADRB1, g.1293C>T and g.1311T>C in ADRB2), four synonymous mutations (g.1054T>C, g.1122C>T and g.1143G>T in ADRB1 and g.506A>G in ADRB3), as well as one mutation in 3'untranslated region (3'UTR) (g.2799G>A in ADRB3). Interestingly, five of them were located in regions predicted to contain multiple repeats of CG nucleotides (CpG islands). Association analysis showed relationships between most of those SNPs or combined haplotypes and carcass traits of Qinchuan cattle. This study association analysis suggests that polymorphisms in these genes might be useful for selection in beef cattle breeding.

Decreased incidence of gout in diabetic patients using pioglitazone.

The incidence and prevalence of gout are increasing, but the management is poor. Considering the increased prevalence of gout in the diabetic population, this study evaluated the effects of pioglitazone, an insulin resistance inhibitor, on the incidence of gout in the diabetic population.

Whole-genome sequencing of African dogs provides insights into adaptations against tropical parasites.

Natural selection in domestic dogs is of great interest in evolutionary biology since dogs have migrated to every inhabited continent of the world alongside humans, and adapted to diverse environments. Here, we explored their demographic history and genetic basis of adaptation to the tropical African environment using whole genome analyses of 19 African indigenous dogs from Nigeria. Demographic analysis suggests that the ancestors of these dogs migrated into Africa from Eurasia 14,000 years ago and underwent a severe founder effect before population expansion. Admixture analysis further reveals that African dog genomes contain about 1.88%-3.50% introgression from African golden wolves (Canis anthus). Population genetic analysis identifies 50 positively selected genes linked with immunity, angiogenesis, ultraviolet protection, as well as insulin secretion and sensitivity that may contribute to adaptation to tropical conditions. One of the positively selected genes, ADGRE1 (adhesion G protein-coupled receptor E1), has also been found to be association with severe malaria resistance in African human populations. Functional assessments showed that ADGRE1 provides protective host defense against Plasmodium infections. This result, together with the fact that the inflammatory response to canine babesiosis is similar to complicated falciparum malaria in humans, support the dogs as a model for the study of malaria control and treatment.

The prevalence of Type 2 diabetes is not increased in normal-weight women with PCOS.

Is oral glucose tolerance test (OGTT) needed in all women with polycystic ovary syndrome (PCOS)?