Read by QxMD icon Read

Journal of Endocrinology

Luba Sominsky, Christine L Jasoni, Hannah Twigg, Sarah J Spencer
The hypothalamus is a key centre for regulation of vital physiological functions, such as appetite, stress responsiveness and reproduction. Development of the different hypothalamic nuclei and its major neuronal populations begins prenatally in both altricial and precocial species, with the fine tuning of neuronal connectivity and attainment of adult function established postnatally, and maintained throughout adult life. The perinatal period is highly susceptible to environmental insults that, by disrupting critical developmental processes, can set the tone for the establishment of adult functionality...
March 15, 2018: Journal of Endocrinology
Michael W Pankhurst, Rebecca L Kelley, Rachel L Sanders, Savana R Woodcock, Dorothy E Oorschot, Nicola J Batchelor
Anti-Müllerian hormone (AMH) is an ovarian regulator that affects folliculogenesis. AMH inhibits the developmental activation of the dormant primordial follicles and the oocyte within. In more mature follicles, AMH reduces granulosa cell sensitivity to follicle-stimulating hormone (FSH). We examined the effects of AMH overexpression on the stages of ovarian folliculogenesis, and the development of embryos, with a transgenic mouse that overexpresses human AMH in central nervous system neurons under the control of the mouse Thy1...
March 14, 2018: Journal of Endocrinology
Min Hu, Yuehui Zhang, Jiaxing Feng, Xue Xu, Jiao Zhang, Wei Zhao, Xiaozhu Guo, Juan Li, Edvin Vestin, Peng Cui, Xin Li, Xiaoke Wu, Mats Brannstrom, Linus R Shao, Hakan Billig
Impaired progesterone (P4) signaling is linked to endometrial dysfunction and infertility in women with polycystic ovary syndrome (PCOS). Here we report for the first time that elevated expression of progesterone receptor (PGR) isoforms A and B parallels increased estrogen receptor (ER) expression in PCOS-like rat uteri. The aberrant PGR-targeted gene expression in PCOS-like rats before and after implantation overlaps with dysregulated expression of Fkbp52 and Ncoa2, two genes that contribute to the development of uterine P4 resistance...
March 13, 2018: Journal of Endocrinology
Claes Ohlsson, Petra Henning, Karin H Nilsson, Jianyao Wu, Karin L Gustafsson, Klara Sjögren, Anna E Törnqvist, Antti Koskela, Fu-Ping Zhang, Marie K Lagerquist, Matti Poutanen, Juha Tuukkanen, Ulf H Lerner, Sofia Movérare-Skrtic
Substantial progress has been made in the therapeutic reduction of vertebral fracture risk in patients with osteoporosis, but non-vertebral fracture risk has been improved only marginally. Human genetic studies demonstrate that the WNT16 locus is a major determinant of cortical bone thickness and non-vertebral fracture risk and mouse models with life-long Wnt16 inactivation revealed that WNT16 is a key regulator of cortical thickness. These studies, however, could not exclude that the effect of Wnt16 inactivation on cortical thickness might be caused by early developmental and/or growth effects...
March 12, 2018: Journal of Endocrinology
Ishita Bakshi, Eurwin Suryana, Lewin Small, Lake Ee Quek, Amanda Brandon, Nigel Turner, Gregory J Cooney
Skeletal muscle is a major tissue for glucose metabolism and can store glucose as glycogen, convert glucose to lactate via glycolysis and fully oxidise glucose to CO2. Muscle has a limited capacity for gluconeogenesis but can convert lactate and alanine to glycogen. Gluconeogenesis requires FBP2, a muscle specific form of fructose bisphosphatase that converts fructose-1,6-bisphosphate (F-1,6-bisP) to fructose-6-phosphate (F-6-P) opposing the activity of the ATP-consuming enzyme phosphofructokinase (PFK). In mammalian muscle, the activity of PFK is normally 100 times higher than FBP2 and therefore energy wasting cycling between PFK and FBP2 is low...
March 5, 2018: Journal of Endocrinology
Sung-Soo Park, Yeon-Joo Lee, Sooyeon Song, Boyong Kim, Hyuno Kang, Sejong Oh, Eungseok Kim
Obesity is a major threat to public health, and it is strongly associated with insulin resistance and fatty liver disease. Here, we demonstrated that administration of Lactobacillus acidophilus NS1 (LNS1) significantly reduced obesity and hepatic lipid accumulation, with a concomitant improvement in insulin sensitivity, in high fat diet (HFD)-fed mice. Furthermore, administration of LNS1 inhibited the effect of HFD feeding on the SREBP-1c and PPARα signaling pathways, and reduced lipogenesis with an increase in fatty acid oxidation in ex vivo livers from HFD-fed mice...
March 5, 2018: Journal of Endocrinology
Sheree Martin, Sean L McGee
A wealth of epidemiological data has found that patients with type 2 diabetes have a greater risk of developing breast cancer. The molecular mechanisms underpinning this relationship are yet to be elucidated, however this review examines the available evidence suggesting that the metabolic abnormalities observed in type 2 diabetes can predispose to the development of breast cancer. Alterations in substrate availability and the hormonal milieu, particularly hyperinsulinemia, not only create a favorable metabolic environment for tumorigenesis, but also induce metabolic reprogramming events that are required for the transformation of breast cancer cells...
February 27, 2018: Journal of Endocrinology
Cyril S Anyetei-Anum, Vincent R Roggero, Lizabeth A Allison
The thyroid hormone receptors, TRα1, TRβ1, and other subtypes, are members of the nuclear receptor superfamily that mediate the action of thyroid hormone signaling in numerous tissues to regulate important physiological and developmental processes. Their most well-characterized role is as ligand-dependent transcription factors; TRs bind thyroid hormone response elements in the presence or absence of thyroid hormone to facilitate the expression of target genes. Although primarily residing in the nucleus, TRα1 and TRβ1 shuttle rapidly between the nucleus and cytoplasm...
February 12, 2018: Journal of Endocrinology
Marleen B Dommerholt, Derek A Dionne, Daria F Hutchinson, Janine K Kruit, James D Johnson
Caloric restriction (CR) is the only environmental intervention with robust evidence that it extends lifespan and delays the symptoms of ageing, but its mechanisms are incompletely understood. Based on the prolonged longevity of knockout models, it was hypothesized that the insulin-IGF pathway could be a target for developing a CR mimic. This study aimed to test whether CR has additive effects on glucose homeostasis and beta-cell function in mice with reduced insulin gene dosage. To study models with a range of basal insulin levels, wildtype C57BL/6J and mice on an Ins2 -/- background, were put on 8 weeks of 40% CR...
February 9, 2018: Journal of Endocrinology
Patricia K Russell, Salvatore Mangiafico, Barbara Fam, Michele Verity Clarke, Evelyn S Marin, Sof Andrikopoulos, Kristine M Wiren, Jeffrey David Zajac, Rachel A Davey
It is well established that testosterone negatively regulates fat mass in humans and mice, however the mechanism by which testosterone exerts these effects is poorly understood. We and others have shown that deletion of the androgen receptor (AR) in male mice results in a phenotype that mimics the three key clinical aspects of hypogonadism in human males; increased fat mass, and decreased bone and muscle mass. We now show that replacement of the AR gene specifically in mesenchymal progenitor cells (PCs) residing in the bone marrow of Global-ARKO mice, in the absence of the AR in all other tissues (PC-AR Gene Replacements), completely attenuates their increased fat accumulation...
January 31, 2018: Journal of Endocrinology
Sung Wook Park, Shawna D Persaud, Stanislas Ogokeh, Tatyana A Meyers, DeWayne Townsend, Li Na Wei
Excessive and/or persistent activation of calcium-calmodulin protein kinase II (CaMKII) is detrimental in acute and chronic cardiac injury. However, intrinsic regulators of CaMKII activity are poorly understood. We find that cellular retinoic acid binding protein 1 (CRABP1) directly interacts with CaMKII, and uncover a functional role for CRABP1 in regulating CaMKII activation. We generated Crabp1 null mice (CKO) in C57BL/6J background for pathophysiological studies. CKO mice develop hypertrophy as adults, exhibiting significant left ventricular dilation with reduced ejection fraction at the baseline cardiac function...
January 25, 2018: Journal of Endocrinology
Hao Wu, Junduo Wu, Shengzhu Zhou, Wenlin Huang, Ying Li, Huan Zhang, Junnan Wang, Ye Jia
Endothelial dysfunction contributes to diabetic macrovascular complications. Sirtuin 1 (SIRT1) protects against diabetic vasculopathy. SRT2104 is a novel SIRT1 activator and was not previously studied for its effects on diabetes-induced aortic endothelial dysfunction. Additionally, whether or to what extent deacetylation of P53, a substrate of SIRT1, is required for the effects of SIRT1 activation was unclear, given the fact that SIRT1 has multiple targets. Moreover, little was known for the pathogenic role of P53 in diabetes-induced aortic injury...
January 25, 2018: Journal of Endocrinology
Adrian Plaza, Beatriz Merino, Victoria Cano, Gema Domínguez, Javier Pérez-Castells, Maria S Fernandez-Alfonso, Coralie Sengenès, Julie A Chowen, Mariano Ruiz-Gayo
The incorporation of plasma triglyceride (TG) fatty acids to white adipose tissue (WAT) depends on lipoprotein lipase (LPL), which is regulated by angiopoietin-like protein-4 (ANGPTL-4), an unfolding molecular chaperone that converts active LPL dimers into inactive monomers. The production of ANGPTL-4 is promoted by fasting and repressed by feeding. We hypothesized that the postprandial hormone cholecystokinin (CCK) facilitates the storage of dietary TG fatty acids in WAT by regulating the activity of the LPL/ANGPTL-4 axis and that it does so by acting directly on CCK receptors in adipocytes...
January 16, 2018: Journal of Endocrinology
Andrea Mafficini, Aldo Scarpa
Neuroendocrine tumours (NETs) may arise throughout the body and are a highly heterogeneous, relatively rare class of neoplasms difficult to study also for the lack of disease models. Despite this, knowledge on their molecular alterations has expanded in the latest years, also building from genetic syndromes causing their onset. Pancreatic NETs (PanNETs) have been among the most studied, and research so far has outlined a series of recurring features, as inactivation of MEN1, VHL, TSC1/2 genes, and hyperactivation of the PI3K/mTOR pathway...
January 10, 2018: Journal of Endocrinology
Salla Nuutinen, Liisa Ailanen, Eriika Savontaus, Petteri Rinne
Atherosclerosis is a chronic inflammatory disease of the arteries. The disease is initiated by endothelial dysfunction that allows the transport of leukocytes and low-density lipoprotein into the vessel wall forming atherosclerotic plaques. The melanocortin system is an endogenous peptide system that regulates, for example, energy homeostasis and cardiovascular function. Melanocortin treatment with endogenous or synthetic melanocortin peptides reduces body weight, protects the endothelium and alleviates vascular inflammation, but the long-term effects of melanocortin system activation on atheroprogression remain largely unknown...
January 9, 2018: Journal of Endocrinology
Min Joo Kim, Se Hee Min, Seon Young Shin, Mi Na Kim, Hakmo Lee, Jin Young Jang, Sun-Whe Kim, Kyong Soo Park, Hye Seung Jung
PERK is a pancreatic endoplasmic reticulum (ER) kinase. Its complete deletion in pancreatic β cells induces insulin deficiency; however, the effects of partial Perk suppression are unclear. We investigated the effect of partial PERK suppression using the specific PERK inhibitors GSK2606414 and GSK2656157. Low dose GSK2606414 treatment for 24 h enhanced glucose-stimulated insulin secretion (GSIS), islet insulin content, and calcium transit in mouse (at 40 nM) and human (at 50~100 nM) pancreatic islets. GSK2606414 also induced the expression of the ER chaperone BiP and the release of calcium from the ER...
December 22, 2017: Journal of Endocrinology
Junhong Chen, Jing Sun, Michelle E Doscas, Jin Ye, Ashley J Williamson, Yanchun Li, Yi Li, Richard A Prinz, Xiulong Xu
p70 S6 kinase (S6K1) is a serine/threonine kinase that phosphorylates the insulin receptor substrate-1 (IRS-1) at serine 1101 and desensitizes insulin receptor signaling. S6K1 hyperactivation due to overnutrition leads to hyperglycemia and type 2 diabetes. Our recent study showed that A77 1726, the active metabolite of the anti-rheumatoid arthritis (RA) drug leflunomide, is an inhibitor of S6K1. Whether leflunomide can control hyperglycemia and sensitize the insulin receptor has not been tested. Here we report that A77 1726 increased AKTS473/T308 and S6K1T389 phosphorylation but decreased S6S235/236 and IRS-1S1101 phosphorylation in 3T3-L1 adipocytes, C2C12 and L6 myotubes...
April 2018: Journal of Endocrinology
Keerati Wanchai, Sakawdaurn Yasom, Wannipa Tunapong, Titikorn Chunchai, Parameth Thiennimitr, Chaiyavat Chaiyasut, Anchalee Pongchaidecha, Varanuj Chatsudthipong, Siriporn Chattipakorn, Nipon Chattipakorn, Anusorn Lungkaphin
Obesity is health issue worldwide, which can lead to kidney dysfunction. Prebiotics are non-digestible foods that have beneficial effects on health. This study aimed to investigate the effects of xylooligosaccharide (XOS) on renal function, renal organic anion transporter 3 (Oat3) and the mechanisms involved. High-fat diet was provided for 12 weeks in male Wistar rats. After that, the rats were divided into normal diet (ND); normal diet treated with XOS (NDX); high-fat diet (HF) and high-fat diet treated with XOS (HFX)...
April 2018: Journal of Endocrinology
Martin Haluzík, Helena Kratochvílová, Denisa Haluzíková, Miloš Mráz
Increasing worldwide prevalence of type 2 diabetes mellitus and its accompanying pathologies such as obesity, arterial hypertension and dyslipidemia represents one of the most important challenges of current medicine. Despite intensive efforts, high percentage of patients with type 2 diabetes does not achieve treatment goals and struggle with increasing body weight and poor glucose control. While novel classes of antidiabetic medications such as incretin-based therapies and gliflozins have some favorable characteristics compared to older antidiabetics, the only therapeutic option shown to substantially modify the progression of diabetes or to achieve its remission is bariatric surgery...
April 2018: Journal of Endocrinology
Malin Fex, Lisa M Nicholas, Neelanjan Vishnu, Anya Medina, Vladimir V Sharoyko, David G Nicholls, Peter Spégel, Hindrik Mulder
Mitochondrial metabolism is a major determinant of insulin secretion from pancreatic β-cells. Type 2 diabetes evolves when β-cells fail to release appropriate amounts of insulin in response to glucose. This results in hyperglycemia and metabolic dysregulation. Evidence has recently been mounting that mitochondrial dysfunction plays an important role in these processes. Monogenic dysfunction of mitochondria is a rare condition but causes a type 2 diabetes-like syndrome owing to β-cell failure. Here, we describe novel advances in research on mitochondrial dysfunction in the β-cell in type 2 diabetes, with a focus on human studies...
March 2018: Journal of Endocrinology
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"