- Serum resistin positively correlates with serum lipids, but not with insulin resistance, in first-degree relatives of type-2 diabetes patients: an observational study in China. [Journal Article]
- MMedicine (Baltimore) 2017; 96(16):e6622
- To investigate whether serum resistin correlated with hypertension, obesity, dyslipidemia, or insulin resistance (IR) in Chinese type 2 diabetes mellitus (T2DM) patients and their first-degree relati...
To investigate whether serum resistin correlated with hypertension, obesity, dyslipidemia, or insulin resistance (IR) in Chinese type 2 diabetes mellitus (T2DM) patients and their first-degree relatives (DFDRs) in a case-control observational study.We determined the serum levels of resistin, plasma lipids, glucose, and insulin, and performed clinical assessments of hypertension, obesity, and IR for 42 T2DM patients, 74 of their DFDRs, and 51 healthy control participants with no family history of T2DM (NC group). The biochemical and clinical variables were compared between the 3 groups, and relationships between serum resistin and the other variables were evaluated using a Pearson correlation analysis.Significant trends were observed in the triglyceride, HbA1c, and resistin levels, in which the values observed in the DFDR group were intermediate to those of the T2DM and NC groups (P < .05 for all). A stratified analysis revealed significant trends in the resistin level and scores for homeostasis model assessment (HOMA) indexes for IR and insulin sensitivity in women and in the HbA1c and resistin levels in men (P < .05 for all), with DFDR subjects exhibiting intermediate values. The Pearson analysis showed that serum resistin positively correlated with total cholesterol and low-density lipoprotein cholesterol in the DFDR group only (P < .05 for both), and that resistin did not correlate significantly with HOMA indexes, blood glucose, insulin, HbA1c, triglyceride, high-density lipoprotein cholesterol, BMI, waist or hip circumference, or blood pressure.Our results suggest that elevated serum resistin might contribute to an increased risk of hyperlipidemia in DFDRs of Chinese T2DM patients.
- Endotext [BOOK]
- BOOKMDText.com, Inc.: South Dartmouth (MA)
- The clinical syndrome of GH deficiency (GHD) is characterised by non-specific features including variable presence of decreased mood and general well-being, reduced bone remodelling activity, change ...
The clinical syndrome of GH deficiency (GHD) is characterised by non-specific features including variable presence of decreased mood and general well-being, reduced bone remodelling activity, change in body fat distribution with increased central adiposity, hyperlipidaemia, and increased predisposition to atherogenesis. The goal of GH replacement therapy in adults with GH deficiency is to correct the wide spectrum of associated clinical alterations. The estimated prevalence of GHD approximates to 2-3:10,000 population. GHD is caused by structural pituitary disease or cranial irradiation, and usually occurs in the context of additional features of hypopituitarism. Pituitary adenomas are the most important cause of adult-onset GHD followed by craniopharyngiomas, which combined account for 57% of cases. Less common causes are irradiation, head injury, vascular, infiltrative, infectious and autoimmune disease. Diagnosing patients with GHD should first of all consider who should be tested for GHD, which includes patients at relevant risk with an intention to treat, next which stimulation test to be used including the proper diagnostic cut-off concentration of GH. The diagnosis of GHD in adults is then usually straightforward. Dosage of h-GH replacement is dependent on age, and gender with adolescents and women usually requiring increased dosage. The dose titration is monitored by IGF-I concentrations and apart from that a number of organ end points, which may act as ‘biomarkers’ of the treatment effects. This document provides an update on GHD including diagnostic pitfalls, and treatment effect, safety and monitoring. For comprehensive coverage of all related areas of Endocrinology please visit our on-line FREE endocrine web-text, WWW.ENDOTEXT.ORG.
- Using Routine Hemoglobin A1c Testing to Determine the Glycemic Status in Psychiatric Inpatients. [Journal Article]
- FEFront Endocrinol (Lausanne) 2017; 8:53
- CONCLUSIONS: Despite relative youth, one-third of all psychiatric inpatients above the age of 30 have diabetes or pre-diabetes. Presence of diabetes in psychiatric inpatients is associated with older age, substance abuse, and longer LOS. Routine inpatient HbA1c testing provides an opportunity for early detection and optimization of diabetes care.
- Anti-obesity effect and protection of liver-kidney functions by Codium fragile sulphated polysaccharide on high fat diet induced obese rats. [Journal Article]
- IJInt J Biol Macromol 2017 Apr 06; 102:119-129
- The present study investigates the hypolipidemic effects of sulphated polysaccharide obtained from Codium fragile (CFSP) in induced obese rats (HFD). The results showed an increase in body weight of ...
The present study investigates the hypolipidemic effects of sulphated polysaccharide obtained from Codium fragile (CFSP) in induced obese rats (HFD). The results showed an increase in body weight of HFD rats by 21.56% as compared to control normal rats. Moreover, serum lipase activity underwent an increase which led to an increase in the levels of total cholesterol (T-Ch), triglycerides (TG) and low density lipoprotein cholesterol (LDL-Ch) in serum associeted with a decrease in the level of high density lipoprotein cholesterol (HDL-Ch) in untreated HFD rats. This diet has disrupted the antioxidant status by decreasing the activities of antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX)) and subsequently an increase in thiobarbituric acid reactive substances (TBARS) level in liver and kidney of obese rats. All these disturbances are significantly corrected by CFSP administration with no fatty deposits in the liver and a protective effect against renal histological alteration. This confirms the important role of this polysaccharide in the fight against oxidative stress and the prevention of hyperlipidemia.
- Lipoprotein-X in cholestatic patients causes xanthomas and promotes foam cell formation in human macrophages. [Journal Article]
- JCJ Clin Lipidol 2017 Jan - Feb; 11(1):110-118
- CONCLUSIONS: This study indicates that Lp-X induces foam cell formation in human-derived macrophages. Our findings strongly suggest that persistently elevated Lp-X may cause xanthomas.
- Estriol: emerging clinical benefits. [Journal Article]
- MMenopause 2017 Apr 03
- CONCLUSIONS: We conclude transvaginal estriol potentially offers a suitable physiologic delivery and cost-effective alternative to currently available estrogen regimens in selected patients. Additional studies on mode of delivery, safety, and efficacy merit further investigation.
- The Associations of Serum Uric Acid with Obesity-Related Acanthosis nigricans and Related Metabolic Indices. [Journal Article]
- IJInt J Endocrinol 2017; 2017:5438157
- CONCLUSIONS: Serum UA levels were positively associated with multiple metabolic abnormalities including obesity, hypertension, hyperglycemia, hyperlipidemia, and AN and may be an important risk factor in the development of AN; further evidences in vitro and in vivo are needed to investigate the direct or indirect relationship.
- Effects of K-877, a novel selective PPARα modulator, on small intestine contribute to the amelioration of hyperlipidemia in low-density lipoprotein receptor knockout mice. [Journal Article]
- JPJ Pharmacol Sci 2017 Feb 11
- Peroxisome proliferator-activated receptor α (PPARα) is a well-known therapeutic target for treating hyperlipidemia. K-877 is a novel selective PPARα modulator (SPPARMα) that enhances PPARα transcrip...
Peroxisome proliferator-activated receptor α (PPARα) is a well-known therapeutic target for treating hyperlipidemia. K-877 is a novel selective PPARα modulator (SPPARMα) that enhances PPARα transcriptional activity with high selectivity and potency, resulting in reduced plasma lipid levels. This study aimed to evaluate the effects of K-877 on hyperlipidemia in low-density lipoprotein receptor knockout (Ldlr(-/-)) mice, a mouse model of atherosclerosis. We revealed that K-877 administration significantly decreased plasma triglyceride (TG) and total cholesterol (TC) levels and increased plasma high-density lipoprotein cholesterol (HDL-C) levels in Ldlr(-/-) mice. K-877 administration to Ldlr(-/-) mice efficiently increased the gene expression of PPARα and its target genes related to fatty acid oxidation in the liver and small intestine. The same treatment significantly increased ATP-binding cassette a1 gene expression in the liver and small intestine and reduced Niemann Pick C1-like 1 gene expression in the small intestine, suggesting that K-877 administration induced HDL-C production in the liver and small intestine and reduced cholesterol absorption in the small intestine. In conclusion, K-877 administration had pronounced effects on the liver and small intestine in Ldlr(-/-) mice. K-877 is an attractive PPARα-modulating drug for treating hyperlipidemia that works equally well in both the liver and small intestine.
- Targeting white, brown and perivascular adipose tissue in atherosclerosis development. [Journal Article]
- EJEur J Pharmacol 2017 Mar 24
- Obesity is a well-established risk factor for atherosclerosis. However, the mechanistic link between accumulation of adipose tissue and development of atherosclerosis is not clear. Adipose tissue com...
Obesity is a well-established risk factor for atherosclerosis. However, the mechanistic link between accumulation of adipose tissue and development of atherosclerosis is not clear. Adipose tissue comprises various depots including white adipose tissue (WAT), brown adipose tissue (BAT) and thoracic and abdominal perivascular adipose tissue (PVAT). The phenotype of thoracic PVAT resembles BAT, whereas abdominal PVAT is more like WAT. Here, we review the distinct roles of the adipose tissue depots in the development of atherosclerosis with the ultimate aim to understand how these can be targeted to reduce atherosclerosis. In obesity, increased fatty acid release by WAT and decreased lipid combustion by BAT and thoracic PVAT lead to hyperlipidaemia, which contributes to atherosclerosis development. Besides, obese WAT and abdominal PVAT release pro-inflammatory factors that further promote atherosclerosis. To discourage atherosclerosis development, strategies that reduce the release of pro-inflammatory factors and fatty acids from WAT and abdominal PVAT, or increase combustion of fatty acids by activation of BAT and thoracic PVAT and beiging of WAT are probably most efficient. Possible therapies could include anti-inflammatory compounds such as adiponectin and salicylates to lower inflammation, and β3-adrenergic receptor activators to increase fatty acid combustion. Additional and more specific strategies to promote fatty acid combustion are currently subject of investigation. In conclusion, different adipose depots differentially affect atherosclerosis development, in which atherosclerosis is promoted by energy-storing adipose depots and attenuated by energy-combusting adipose tissue. In obesity, combining therapies that reduce inflammation and increase combustion of lipids are most conceivable to restrain atherogenesis.
New Search Next
- The metabolic ER stress sensor IRE1α suppresses alternative activation of macrophages and impairs energy expenditure in obesity. [Journal Article]
- NINat Immunol 2017; 18(5):519-529
- Obesity is associated with metabolic inflammation and endoplasmic reticulum (ER) stress, both of which promote metabolic disease progression. Adipose tissue macrophages (ATMs) are key players orchest...
Obesity is associated with metabolic inflammation and endoplasmic reticulum (ER) stress, both of which promote metabolic disease progression. Adipose tissue macrophages (ATMs) are key players orchestrating metabolic inflammation, and ER stress enhances macrophage activation. However, whether ER stress pathways underlie ATM regulation of energy homeostasis remains unclear. Here, we identified inositol-requiring enzyme 1α (IRE1α) as a critical switch governing M1-M2 macrophage polarization and energy balance. Myeloid-specific IRE1α abrogation in Ern1(f/f); Lyz2-Cre mice largely reversed high-fat diet (HFD)-induced M1-M2 imbalance in white adipose tissue (WAT) and blocked HFD-induced obesity, insulin resistance, hyperlipidemia and hepatic steatosis. Brown adipose tissue (BAT) activity, WAT browning and energy expenditure were significantly higher in Ern1(f/f); Lyz2-Cre mice. Furthermore, IRE1α ablation augmented M2 polarization of macrophages in a cell-autonomous manner. Thus, IRE1α senses protein unfolding and metabolic and immunological states, and consequently guides ATM polarization. The macrophage IRE1α pathway drives obesity and metabolic syndrome through impairing BAT activity and WAT browning.