inflammatory processes in adipose tissue ( 5 ). It is crucial to understand the metabolism and targeted effects of vitamin D and especially how these are affected in obesity. To date, we know that vitamin D supplementation increases circulating 25-OHD in
Elisabet Einarsdottir, Minna Pekkinen, Kaarel Krjutškov, Shintaro Katayama, Juha Kere, Outi Mäkitie, and Heli Viljakainen
Masatada Watanabe, Shuji Ohno, and Hiroshi Wachi
adrenomedullary system to stress in patients with atopic dermatitis . Journal of Clinical Endocrinology and Metabolism 2002 87 4245 – 4251 . ( doi:10.1210/jc.2001-010872 ) 19 Watanabe M Nakajin S. Forskolin up-regulates aromatase (CYP19) activity
Dmitry M Davydov and Malik K Nurbekov
status in individuals with and without type 2 diabetes (e.g., altered erythrocyte physiology), individual variance in both glycemic parameters can reflect different aspects of energy metabolism that are modulated by different gene polymorphisms. However
Julia Kubiak, Per Medbøe Thorsby, Elena Kamycheva, and Rolf Jorde
HOMA-IR values above the median for the cohort, combined with low baseline serum 25(OH)D; but again, no significant effects of vitamin D were found. Previous studies on vitamin D and lipid and glucose metabolism have generally included standard
Piera Rizzolo, Valentina Silvestri, Virginia Valentini, Veronica Zelli, Agostino Bucalo, Ines Zanna, Simonetta Bianchi, Maria Grazia Tibiletti, Antonio Russo, Liliana Varesco, Gianluca Tedaldi, Bernardo Bonanni, Jacopo Azzollini, Siranoush Manoukian, Anna Coppa, Giuseppe Giannini, Laura Cortesi, Alessandra Viel, Marco Montagna, Paolo Peterlongo, Paolo Radice, Domenico Palli, and Laura Ottini
in genes involved in estrogen biosynthesis and metabolism pathways, such as Cytochrome P450 family 17 subfamily A member 1 ( CYP17A1 ) and Cytochrome P450 family 1 subfamily B member 1 ( CYP1B1 ), may cause an increased risk of hormone-related cancers
Masafumi Tetsuka and Misato Tanakadate
the local glucocorticoid environment in the bovine COC is eloquently regulated during oocyte maturation. The physiological significance of the HSD11B-led glucocorticoid metabolism in the oocyte maturation has not yet been clarified. However, it is
Taís S Assmann, Mariana Recamonde-Mendoza, Bianca M De Souza, and Daisy Crispim
regulation of various processes, such as cellular differentiation, proliferation, metabolism, aging and apoptosis ( 10 , 12 ). miRNAs are estimated to regulate the expression of more than 60% of protein-coding genes ( 9 ); consequently, changes in their
Wang Chengji and Fan Xianjin
Endocrinology and Metabolism 2007 21 573 – 586 . ( https://doi.org/10.1016/j.beem.2007.09.007 ) 10.1016/j.beem.2007.09.007 39 Kleindienst A Battault S Belaidi E Tanguy S Rosselin M Boulghobra D
Riying Liang, Meijun Wang, Chang Fu, Hua Liang, Hongrong Deng, Ying Tan, Fen Xu, and Mengyin Cai
Background: Obesity is associated with the development and progression of chronic kidney disease. Emerging evidence suggests that glucagon-like peptide-1 receptor agonist could reduce renal damage and albuminuria. Sirtuin 1 (SIRT1) was considered as a crucial regulator in metabolism-related kidney disease. Herein, the role of SIRT1 in liraglutide-ameliorated high-fat diet (HFD)-induced kidney injury was illustrated.
Methods: Male C57BL/6 mice were fed HFD for 20 weeks to induce kidney injury that was then treated with liraglutide for 8 weeks to estimate its protective effect on the kidney. Also, the mechanism of the drug in SV40 MES 13 (SV40) mouse mesangial cells was elucidated.
Results: Liraglutide treatment ameliorated HFD-induced metabolic disorders, including hyperglycemia, increasing body weight, and insulin resistance. In addition, kidney weight, urine albumin-to-creatinine, and kidney morphological changes such as vacuolated tubules, glomerulomegaly, thickened glomerular basement membrane, and tubulointerstitial fibrosis were also significantly ameliorated. Furthermore, apoptotic cells and apoptosis markers were downregulated in the kidney of liraglutide-treated mice. In addition, the expression of SIRT1 protein was upregulated, whereas thioredoxin-interacting protein (TXNIP), which serves as a mediator of oxidative stress and apoptosis in metabolism disease, was downregulated by liraglutide. In SV40 cells, the effect of liraglutide on reversing the upregulation of cleaved caspase-3 induced by high glucose (30 mM) was hampered when SIRT1 was knocked down; also, the downregulation of TXNIP by liraglutide was blocked.
Conclusions: Liraglutide might have a beneficial effect on metabolism-related kidney damage by inhibiting apoptosis via activation of SIRT1 and suppression of TXNIP pathway.
Lina Susana Silva-Bermudez, Freddy Jk Toloza, Maria Camila Perez-Matos, Russell J de Souza, Laura Banfield, Andrea Vargas-Villanueva, and Carlos O Mendivil
Objective: To estimate the effect of oral contraceptives (OC) containing different progestins on parameters of lipid and carbohydrate metabolism through a systematic review and meta-analysis.
Patients and Methods: Premenopausal women aged 18 or older, who received oral contraceptives containing chlormadinone, cyproterone, drospirenone, levonorgestrel, desogestrel, dienogest, gestodene or norgestimate, for at least 3 months. Outcome variables were changes in plasma lipids, body-mass index (BMI), insulin resistance and plasma glucose. We searched MEDLINE and EMBASE for randomized trials and estimated the pooled within-group change in each outcome variable using a random effects model. We performed subgroup analyses by study duration (<12 months versus ˃=12 months) and polycystic ovary syndrome status.
Results: Eighty-two clinical trials fulfilled the inclusion criteria. All progestins (except dienogest) increased plasma TG, ranging from 12.1 mg/dL for levonorgestrel (p<0.001) to 35.1 mg/dL for chlormadinone (p<0.001). Most progestins also increased HDLc, with the largest effect observed for chlormadinone (+9.6 mg/dL, p<0.001) and drospirenone (+7.4 mg/dL, p<0.001). Meanwhile, levonorgestrel decreased HDLc by 4.4 mg/dL (p<0.001). Levonorgestrel (+6.8 mg/dL, p<0.001) and norgestimate (+11.5 mg/dL, p=0.003) increased LDLc, while dienogest decreased it (-7.7 mg/dL, p=0.04). Cyproterone slightly reduced plasma glucose. None of the progestins affected BMI or HOMA-IR. Similar results were observed in subgroups defined by PCOS or study duration.
Conclusion: Most progestins increase both TG and HDLc, their effect on LDLc varies widely. OC have minor or no effects on BMI, HOMA-IR and glycemia. The antiandrogen progestins dienogest and cyproterone displayed the most favorable metabolic profile, while levonorgestrel displayed the least favorable.