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Endocrinology AND Hyperlipidemia [keywords]
- Differences in cholesterol management among states in relation to health insurance and race/ethnicity across the United States. [Journal Article]
- J Clin Lipidol 2013 Nov-Dec; 7(6):675-82.
Across the United States, hyperlipidemia remains inadequately controlled and may vary across states according to differences in health insurance coverage and/or race/ethnicity.To examine relationships between states' health insurance and race/ethnicity characteristics with measures of hyperlipidemia management across the 50 U.S. states and the District of Columbia.Cross-validated, multiple linear regression modeling was used to analyze associations between states' health insurance patterns or proportions of racial minorities (from the 2010 U.S. Census data) and states' aggregate frequency of checking cholesterol within the previous 5 years or prescriptions written for lipid-lowering medications (from national survey and population-adjusted retail prescription data, respectively), with adjustments for age, sex, body mass index, race/ethnicity, and poverty.In states with proportionately more uninsured, cholesterol levels are checked less often, but in states with proportionately more private, Medicare, or Medicaid coverage, providers are not necessarily more likely to check cholesterol or to write more prescriptions. In states with proportionately more African-Americans and/or Hispanics, cholesterol is more likely to be checked, but in states with more African-Americans, more prescriptions were written, whereas in states with more Hispanics, fewer statin prescriptions were written.Variations across states in insurance and racial/ethnicity mix are associated with variations in hyperlipidemia management; less-insured states may be less effective whereas states with more private, Medicare, or Medicaid coverage may not be more effective. In states with proportionately more African-Americans vs. Hispanics, lipid medications may be prescribed differently. Our findings warrant further investigations.
- Inherited lipemic splenomegaly and the spectrum of apolipoprotein E p.Leu167del mutation phenotypic variation. [Journal Article]
- J Clin Lipidol 2013 Nov-Dec; 7(6):566-72.
We review disorders associated with splenomegaly and dyslipidemia with an emphasis on the APOE p.Leu167del mutation. Recent studies suggest that this rare mutation may present more often without splenomegaly in patients with familial combined hyperlipidemia or autosomal dominant hypercholesterolemia. We supplement the literature review by reporting a new kindred.We reviewed our 3405-patient lipid clinic database to identify persons with dyslipidemia and splenomegaly. Identified patients were evaluated for relevant disorders, including genetic testing for a 3-base pair deletion in APOE that causes deletion of leucine at position 167 of apolipoprotein E.We identified 4 patients with splenomegaly and dyslipidemia, one of whom had a heterozygous APOE p.Leu167del mutation. This proband is a 76-year-old man with a history of splenomegaly first noted at age 13 and subsequent diagnosis of hypertriglyceridemia, low high-density lipoprotein cholesterol, leukopenia, and thrombocytopenia in his third decade. He never required splenectomy, and his splenic enlargement regressed over time with medical management of his hypertriglyceridemia. The APOE p.Leu167del mutation was also found in the proband's son and granddaughter, neither of whom has splenomegaly or marked dyslipidemia.Splenomegaly in association with dyslipidemia may indicate the presence of an underlying disorder. We discuss possible causes, review the literature relating to the rare APOE p.Leu167del mutation, and present a 3-generation kindred with variable phenotypic expression of this mutation. Severity of expression may depend on genotype, sex, or effective medical management of dyslipidemia or a combination of these factors. Aggressive lipid treatment may improve or prevent splenomegaly among patients with this disorder.
- Association of RXR-Gamma Gene Variants with Familial Combined Hyperlipidemia: Genotype and Haplotype Analysis. [Journal Article]
- J Lipids 2013.:517943.
Background.Familial combined hyperlipidemia (FCHL), the most common genetic form of hyperlipdemia, is characterized by a strong familial clustering and by premature coronary heart disease. The FCHL locus has been mapped to human chromosome 1q21-q23. This region includes the retinoid X receptor gamma (RXRG), a nuclear factor member of the RXR superfamily, which plays important roles in lipid homeostasis.
Objective.To investigate the possible role of the RXRG gene in the genetic susceptibility to FCHL. Methods. Variations in RXRG gene were searched by direct sequencing, and the identified SNPs were genotyped by PCR-RFLP in 192 FCHL individuals from 74 families and in 119 controls.
Results.We identified 5 polymorphisms in the RXRG gene (rs1128977, rs2651860, rs2134095, rs283696, and rs10918169). Genotyping showed that the A-allele of rs283696 SNP was significantly associated with FCHL (corrected P, P c < 0.01). Also the alleles of the rs10918169 and of the rs2651860 SNP were more frequent in FCHL subjects compared to those in controls, although not significantly after correction. When the clinical characteristics of the FCHL subjects were stratified by allele carrier status for each SNP, the rs2651860 SNP was significantly associated with increased levels of LDL-cholesterol and of Apo-B in T-allele carriers (P < 0.04). Finally, haplotypes analysis with all 5 SNPs confirmed the significant association of RXRG gene with FCHL. Specifically, the haplotype containing all 3 "at-risk" alleles, significantly associated with FCHL (A-allele of rs283696, G-allele of rs10918169, and T-allele of rs2651860), showed an OR (Odds Ratio) of 2.02, P c < 0.048. Conversely, the haplotype without all these 3 alleles was associated with a reduced risk for FCHL (OR = 0.39, P c < 0.023). The "at-risk" haplotype CTTAG was also associated with higher LDL-C (P < 0.015). In conclusion, variation in the RXRG gene may contribute to the genetic dyslipidemia in FCHL subjects.
- [Acquired hypertriglyceridemia]. [English Abstract, Journal Article]
- Nihon Rinsho 2013 Sep; 71(9):1597-601.
Hypertriglyceridemia is associated with an increase in very low density lipoprotein (VLDL), chylomicron, intermediate density lipoprotein(IDL). Acquired hyperlipidemia results from various disorders, such as obesity, diabetes mellitus, alcohol overuse, chronic kidney disease, hypothyroidism, and some drugs like thiazide, -blocker, estrogen, etc. It is important to identify secondary causes underlying hypertriglyceridemia before initiating pharmacotherapy, since management of the causative disorders is the first-line therapy. Even if hyperlipidemia is not controlled after treating the underlying disorders, specific lipid -lowering therapy may be required in addition to lifestyle modification. Fibrate, nicotinic acid and eicosapentaenoic acid are utilized to reduce triglyceride levels. Statin and ezetimibe are utilized if non-high density lipoprotein(HDL)-cholesterol is elevated.
- Analysis on traditional Chinese medicine syndrome elements and relevant factors for senile diabetes. [Journal Article, Research Support, Non-U.S. Gov't]
- J Tradit Chin Med 2013 Aug; 33(4):473-8.
To explore the laws governing the distribution of Traditional Chinese Medicine (TCM) syndrome elements (SEs) of senile diabetes (SD) and their relationship to relevant factors.An investigation of patients who met the inclusion criteria was conducted by trained doctors, using case report forms. All related data were collected, including body mass index, glycated hemoglobin, illness course, complications, symptoms, and tongue and pulse manifestation. The SEs of each patient were judged by three qualified associate chief physicians independently.The main SEs of SD are Yin deficiency, Qi deficiency, blood stasis, and phlegm turbidity. Yin deficiency, Qi deficiency, blood stasis, and phlegm turbidity are most commonly seen among 4-SE combinations. Yang deficiency is typically related to illness course and BMI, phlegm turbidity to hypertension and hyperlipidemia, excessive heat to diabetic microangiopathy, and blood stasis to illness course and diabetic macroangiopathy.SD pathogenesis has a deficiency in origin and excess in superficiality. Deficiency syndrome mainly manifests as deficiency of both Qi and Yin, and concurrently in Yang deficiency. Excess syndrome is characterized by blood stasis and phlegm turbidity. SEs analysis provides a basis for the prevention and treatment of SD with TCM and lays the foundation for objectively evaluating multicentric clinical research for SD in TCM.
- The effect of pioglitazone and extended-release niacin on HDL-cholesterol in diabetes patients in a real-world setting. [Journal Article]
- Int J Clin Pract 2013 Nov; 67(11):1151-8.
This retrospective study was designed to assess the effects of the combination of pioglitazone and extended-release niacin on the lipid panel, particularly HDL-cholesterol, when used in patients with type 2 diabetes in an endocrinology specialty practice.The electronic medical records of 434 adult patients with type 2 diabetes receiving extended-release niacin and pioglitazone were screened for review. Patients with type 2 diabetes and hyperlipidemia were included for review if they received the combination of pioglitazone at doses ≥ 15 mg/day and extended-release niacin (Niaspan) at doses ≥ 1000 mg/day for ≥6 months. Statistical analysis used paired t-tests with p < 0.05 as statistically significant. Both ANOVA and the Tukey-Kramer test for multiple comparisons (α = 0.05) were also used.A total of 47 patients, 83% were men with average age of 58, met all eligibility criteria for the study. Compared with baseline, a statistically significant increase in HDL-C (+ 25.13%, p < 0.0001) was observed at the conclusion of combination therapy. The HDL-C levels progressively increased with duration of combination treatment, and were not correlated with concomitant statin use. Significant decreases in total cholesterol and triglycerides were detected, and HbA1c decreased 0.84% during combination therapy for all therapies combined.The combination of pioglitazone and extended-release niacin in patients with type 2 diabetes and hyperlipidemia, used in commonly prescribed doses for at least 6 months, resulted in statistically significant improvements in HDL-C, total cholesterol, and triglycerides, and did not result in deteriorations in glycemic control.
- Prevention of Diet-Induced Hyperlipidemia and Obesity by Caffeic Acid in C57BL/6 Mice through Regulation of Hepatic Lipogenesis Gene Expression. [Journal Article]
- J Agric Food Chem 2013 Nov 20; 61(46):11082-8.
This study investigated the influence of phenolic caffeic acid on obesity in mice fed a high fat diet and its underlying mechanisms base on adipose and hepatic lipid lipogenesis. C57BL/6 mice were fed a normal diet or a HFD (20% fat, w/w) with or without caffeic acid (0.02% and 0.08%, w/w) for 6 weeks. The effects of caffeic acid on hyperlipidemia, hyperglycemia, visceral fat accumulation, and related enzyme activities in HFD-mice are examined. The supplementation of caffeic acid significantly lowered body weight, visceral fat mass, plasma GOT and GPT levels, FAS activity, and free fatty acid compared to the HFD group. Caffeic acid also lowered triglyceride and cholesterol concentrations in plasma and liver. Furthermore, we showed that caffeic acid efficiently inhibited cholesterol biosynthesis as evidenced by 3-hydroxy-3-methylglutaryl CoA reductase in the liver. Caffeic acid supplementation suppressed the activity of lipogenesis via sterol regulatory element-binding protein 1 c and its target enzyme fatty acid synthase. In addition, caffeic acid resulted in increased phosphorylation of AMP-activated protein kinase and decreased acetyl carboxylase, a downstream target of AMPK, which are related to fatty acid β-oxidation in the liver. In conclusion, these results indicate that caffeic acid exhibits a significant potential as an antiobesity agent by suppression of lipogenic enzymes and hepatic lipid accumulation.
- Insulin and IGFs in Obesity-Related Breast Cancer. [Journal Article]
- J Mammary Gland Biol Neoplasia 2013 Dec; 18(3-4):277-89.
Obesity and the Metabolic Syndrome are associated with multiple factors that may cause an increased risk for cancer and cancer-related mortality. Factors involved include hyperinsulinemia, hyperglycemia, hyperlipidemia and IGFs. Insulin resistance is also associated with alterations in the levels of proinflammatory cytokines, chemokines, adipokines (leptin, adiponectin) that may also be contributing factors. The insulin family of proteins is ubiquitously expressed and has pleiotropic effects on metabolism and growth. However insulin, IGF-1 and particularly IGF-2 have been identified as tumor promoters in multiple studies. Mouse models have focused on insulin and IGF-1 and their receptors as being involved in tumor progression and metastases. The role of the insulin receptor as either mediating the effects on tumors or as compensating for the insulin-like growth factor receptor has arisen. Its role has been supported by preclinical studies and the importance of insulin resistance and hyperinsulinemia in obesity and early diabetes. Since the focus of this review is the insulin-family we will focus on insulin, IGF-1 and IGF-2.
- Radical roles for RAGE in the pathogenesis of oxidative stress in cardiovascular diseases and beyond. [Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.]
- Int J Mol Sci 2013; 14(10):19891-910.
Oxidative stress is a central mechanism by which the receptor for advanced glycation endproducts (RAGE) mediates its pathological effects. Multiple experimental inquiries in RAGE-expressing cultured cells have demonstrated that ligand-RAGE interaction mediates generation of reactive oxygen species (ROS) and consequent downstream signal transduction and regulation of gene expression. The primary mechanism by which RAGE generates oxidative stress is via activation of NADPH oxidase; amplification mechanisms in the mitochondria may further drive ROS production. Recent studies indicating that the cytoplasmic domain of RAGE binds to the formin mDia1 provide further support for the critical roles of this pathway in oxidative stress; mDia1 was required for activation of rac1 and NADPH oxidase in primary murine aortic smooth muscle cells treated with RAGE ligand S100B. In vivo, in multiple distinct disease models in animals, RAGE action generates oxidative stress and modulates cellular/tissue fate in range of disorders, such as in myocardial ischemia, atherosclerosis, and aneurysm formation. Blockade or genetic deletion of RAGE was shown to be protective in these settings. Indeed, beyond cardiovascular disease, evidence is accruing in human subjects linking levels of RAGE ligands and soluble RAGE to oxidative stress in disorders such as doxorubicin toxicity, acetaminophen toxicity, neurodegeneration, hyperlipidemia, diabetes, preeclampsia, rheumatoid arthritis and pulmonary fibrosis. Blockade of RAGE signal transduction may be a key strategy for the prevention of the deleterious consequences of oxidative stress, particularly in chronic disease.
- Increased resistin serum concentrations in patientswith type 1 diabetes mellitus. [Journal Article]
- J Clin Res Pediatr Endocrinol 2013 Sep 10; 5(3):189-93.
Adiponectin, leptin, and resistin are adipokines which play a significant role in the regulation of lipid and carbohydrate metabolism in patients with type 2 diabetes, while little is known about their role in type 1 diabetes mellitus (T1DM). The aim of this study was to measure serum adiponectin, leptin, and resistin levels and to investigate their relationships with some parameters in patients with T1DM and healthy controls.Fifty children and adolescents with T1DM (21 boys and 29 girls) and 33 healthy control subjects (18 boys and 15 girls) participated in the study. All subjects were patients followed in the Pediatric Endocrinology and Metabolism Unit of Gaziantep University Faculty of Medicine. None of the subjects had hypertension, obesity, hyperlipidemia, anemia, or infection. Adiponectin, leptin, and resistin levels were analyzed with ELISA.There were no statistically significant differences related with age, sex, pubertal status, or body mass index distribution between the diabetic and control groups. Resistin levels were significantly higher in the diabetic group compared to controls (5.26±3.15 ng/mL vs. 3.50±1.26 ng/mL; p<0.01).Of the three investigated adipokines, only resistin was associated with T1DM. Resistin may play a role in the process of inflammation and also in the pathophysiology of T1DM.