(Endocrinology AND Hyperlipidemia)
- Chemical Hybridization of Glucagon and Thyroid Hormone Optimizes Therapeutic Impact for Metabolic Disease. [Journal Article]
- CellCell 2016 Oct 20; 167(3):843-857.e14
- Glucagon and thyroid hormone (T3) exhibit therapeutic potential for metabolic disease but also exhibit undesired effects. We achieved synergistic effects of these two hormones and mitigation of their...
Glucagon and thyroid hormone (T3) exhibit therapeutic potential for metabolic disease but also exhibit undesired effects. We achieved synergistic effects of these two hormones and mitigation of their adverse effects by engineering chemical conjugates enabling delivery of both activities within one precisely targeted molecule. Coordinated glucagon and T3 actions synergize to correct hyperlipidemia, steatohepatitis, atherosclerosis, glucose intolerance, and obesity in metabolically compromised mice. We demonstrate that each hormonal constituent mutually enriches cellular processes in hepatocytes and adipocytes via enhanced hepatic cholesterol metabolism and white fat browning. Synchronized signaling driven by glucagon and T3 reciprocally minimizes the inherent harmful effects of each hormone. Liver-directed T3 action offsets the diabetogenic liability of glucagon, and glucagon-mediated delivery spares the cardiovascular system from adverse T3 action. Our findings support the therapeutic utility of integrating these hormones into a single molecular entity that offers unique potential for treatment of obesity, type 2 diabetes, and cardiovascular disease.
- Comparison of Optimal Cardiovascular Risk Factor Management in Patients with Type 2 Diabetes Who Attended Urban Medical Health Center with those Attended a Tertiary Care Center: Experiences from Tehran, Iran. [Journal Article]
- IJInt J Prev Med 2016; 7:113
- CONCLUSIONS: Both centers have failure in target achievement in some risk factors; however, the inability of the primary care center in controlling hyperlipidemia in comparison with the tertiary center is a serious warning to provide training about managing dyslipidemia in these centers.
- [Woman 19-old with hirsutism, obesity and acanthosis nigricans]. [Journal Article]
- PMPol Merkur Lekarski 2016 Sep 29; 41(243):141-144
- 19-year-old hirsute woman with obesity, skin lesions with features of acanthosis nigricans around neck, armpits, thoracic cage and wrists escalating for couple of months, elevated testosterone and in...
19-year-old hirsute woman with obesity, skin lesions with features of acanthosis nigricans around neck, armpits, thoracic cage and wrists escalating for couple of months, elevated testosterone and insulin plasma levels was admitted to hospital to perform diagnostic approach. The final diagnosis was hyperandrogenism-insulin resistance-acanthosis nigricans syndrome (HAIR-AN syndrome), considered as a subtype of policystic ovary syndrome (PCOS) and impaired glucose tolerance. HAIR-AN is characterized by coexistence of: hyperandrogenism (HA), insulin resistance (IR) and acanthosis nigricans (AN). These symptoms are result of increased insulin and androgens levels. Due to accompanying complications (obesity, hyperglycemia, hyperlipidemia, infertility) patients with HAIR-AN syndrome should be monitored and treated. Rarely acanthosis nigricans, especially when occurs rapidly and extensively, may be a paraneoplastic disorder. Life style modification with BMI reduction was recommended and metformin, a drug improving sensitivity to insulin, was administered. Patient should be monitored due to possible complications of obesity, diabetes and hyperinsulinemia.
- The Diagnosis and Management of Lipodystrophy Syndromes: A Multi-Society Practice Guideline. [Journal Article]
- JCJ Clin Endocrinol Metab 2016 Oct 6; :jc20162466
- CONCLUSIONS: Lipodystrophy syndromes are heterogeneous, and are diagnosed by clinical phenotype, supplemented by genetic testing in certain forms. Patients with most lipodystrophy syndromes should be screened for diabetes, dyslipidemia, and liver, kidney, and heart disease annually. Diet is essential for management of metabolic complications of lipodystrophy. Metreleptin therapy is effective for metabolic complications in hypoleptinemic patients with generalized lipodystrophy, and selected patients with partial lipodystrophy. Other treatments not specific for lipodystrophy may be helpful as well (e.g. metformin for diabetes, statins or fibrates for hyperlipidemia). Oral estrogens are contraindicated.
- Accelerated Accumulation of Multimorbidity After Bilateral Oophorectomy: A Population-Based Cohort Study. [Journal Article]
- MCMayo Clin Proc 2016 Sep 28
- CONCLUSIONS: Bilateral oophorectomy is associated with a higher risk of multimorbidity, even after adjustment for conditions present at baseline and for several possible confounders. However, several of these associations were reduced in women who received estrogen therapy.
- The very high cardiovascular risk in heterozygous familial hypercholesterolemia: Analysis of 734 French patients. [Journal Article]
- JCJ Clin Lipidol 2016 Sep-Oct; 10(5):1129-1136.e3
- CONCLUSIONS: This study provides a detailed description of French heFH patients according to their CV risk. Patients with very high CV risk had usually more advanced carotid plaques and were treated with heavier lipid-lowering drugs although their LDL-C level remained similar. This highlights the significant burden of this population.
- Reduced femoral bone mass in both diet-induced and genetic hyperlipidemia mice. [Journal Article]
- BONEBone 2016 Sep 23; 93:104-112
- Growing evidence argues for a relationship between lipid and bone metabolisms with inconsistent conclusions. Sphingosine-1-phosphate (S1P) has been recognized as a suitable candidate for possible lin...
Growing evidence argues for a relationship between lipid and bone metabolisms with inconsistent conclusions. Sphingosine-1-phosphate (S1P) has been recognized as a suitable candidate for possible link between lipid metabolism and bone metabolism. This study was designed to investigate the effects of hyperlipidemia on bone metabolism using diet-induced and genetic-induced hyperlipidemia animal models and to explore whether S1P is involved. Wild-type mice and low-density lipoprotein receptor gene deficient (LDLR(-/-)) mice at age of 8weeks were placed on either control diet or high-fat diet (HFD) for 12weeks. Bone structural parameters were determined using microCT. Cross-linked type I collagen (CTx) and S1P levels in plasma were measured by ELISA methods. Bone marrow cells from wild type and LDLR(-/-) mice were induced to differentiate into osteoblasts, osteoclasts and adipocytes respectively. Gene expressions in distal femur metaphyses and cultured cells were studied by qRT-PCR. Moderate hypercholesterolemia was found in HFD-feeding mice; severe hypercholesterolemia and moderate hypertriglyceridemia were present in LDLR(-/-) mice. Femoral trabecular bone mass was reduced in both diet-induced and genetic hyperlipidemia mice. Mice feeding on HFD showed higher CTx levels, and mice with hyperlipidemia had elevated S1P levels. Correlation analysis found a positive correlation between CTx and S1P levels. Lower Runx2 expression and higher TRAP expression were found in both diet-induced and genetic hyperlipidemia mice, indicating decreased osteoblastic functions and increased osteoclastic functions in these mice. Bone marrow cells from LDLR(-/-) mice also showed increased adipogenesis and inhibited osteogenesis accompanied by enhanced PPARγ expression. In conclusion, our study found decreased bone mass in both diet-induced and genetic hyperlipidemia mice.
- Effects of hyperlipidaemia on plasma apolipoprotein M levels in patients with type 2 diabetes mellitus: an independent case-control study. [Journal Article]
- LHLipids Health Dis 2016 Sep 15; 15(1):158
- CONCLUSIONS: Plasma apoM concentrations are higher in patients with hyperlipidaemia than in healthy controls. Low plasma apoM levels in patients with T2DM are likely caused by diabetes but are not induced by hyperlipidaemia.
- Exploring Inpatient Hospitalizations and Morbidity in Patients with Adrenal Insufficiency. [Journal Article]
- JCJ Clin Endocrinol Metab 2016 Sep 13; :jc20162221
- CONCLUSIONS: Patients with AI carry a significant metabolic and psychiatric burden, with higher risk of comorbidities and hospital admissions than matched controls. Secondary abstract This retrospective observational study using data from a US-based national payer database showed patients with adrenal insufficiency to be at increased risk of comorbid conditions and hospitalization compared to matched controls.
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- Angiopoietin-like protein 4 improves glucose tolerance and insulin resistance but induces liver steatosis in high-fat-diet mice. [Journal Article]
- MMMol Med Rep 2016; 14(4):3293-300
- Angiopoietin-like protein 4 (Angptl4) is a secreted protein predominantly expressed in liver and adipose tissues, and has been identified as an adipokine. Angptl4 is the target gene of peroxisome pro...
Angiopoietin-like protein 4 (Angptl4) is a secreted protein predominantly expressed in liver and adipose tissues, and has been identified as an adipokine. Angptl4 is the target gene of peroxisome proliferator‑activated receptors, which are widely used as lipid‑lowering and anti‑diabetic drugs, and previous studies have demonstrated that Angptl4 is able to directly stimulate adipocyte lipolysis. The current study focused on how Angptl4 was involved in regulating lipid and glucose metabolism in high‑fat‑diet (HFD) C57 mice. In the present study, mice were divided into three groups, with standard chow mice as a normal control, adenovirus (adv)‑injected HFD mice as a model control and adv‑Angptl4‑injected HFD mice as the Angptl4+ group. Firstly, compared with the normal control group, mice in the model control group gained more body weight with severe liver steatosis and increased serum levels of triglyceride, total cholesterol, free fatty acids, alanine aminotransferase and aspartate aminotransferase. In the Angptl4+ group, Angptl4 reduced the weight growth rate, aggravated hepatic steatosis and further increased all the aforementioned serum indexes. Secondly, compared with the normal control, the model control group had a reduced glucose tolerance and developed insulin resistance. Angptl4 expression and the phosphorylation levels of several insulin signaling pathway‑associated genes, insulin receptor substrate 1, protein kinase B, janus kinase 2, signal transducer and activator of transcription 3 were downregulated in the liver samples. Adv‑Angptl4 injection was observed to improve glucose tolerance and insulin resistance. The genes measured were identified to be upregulated close to normal levels. All the results suggested that Angptl4 served an important role in lipid and glucose metabolism in HFD‑induced obese mice, and this may have a great significance for treatment of hyperlipidemia, diabetes, metabolic syndrome and other diseases.