Reproductive endocrinology provides us with a lot of tips in a various area of medical science. In this issue, Dr. Tamura and colleague contribute an insightful review article focusing on glucose and lipid metabolism in human endometrial stromal cells during the course of decidualization. To effectively supply energy for embryo, human endometrial stromal cells aggressively ingest fuel via GLUT1 and VLDL receptor under the transcriptional control and epigenetic modification involved in C/EBP beta, p300 and WT1. Such a fashion would be reminiscent, at least in part, of fuel metabolism commonly seen in cancer cells. It is also anticipated that energy metabolism-based unique approach in this article opens a fresh avenue for cutting edge medicine and therapeutics on incomplete implantation or infertility.
As well known, comparative endocrinology has long provided deep insight into pathophysiology and molecular basis of a variety of human endocrinologic diseases. In this issue, by use of a small fish model, Dr. Yoshitaka Oka contributes an extensive, well-organized article on the recent research progress in neuroendocrine regulation of reproduction by GnRH neurons, providing us with an invaluable perspective for cutting-edge area of reproductive endocrinology in humans.
It is well recognized that a line of symptoms of neurohypophyseal diabetes insipidus (NDI), also known as arginine vasopressin (AVP) deficiency, are masked under the condition of adrenal insufficiency. However, molecular mechanisms whereby polyuria manifests after the administration of glucocorticoids in patients with masked NDI have not been fully elucidated. Kurimoto J and colleague elegantly solved this long-lasting enigma via comprehensive analyses including patients with masked NDI as well as murine model of familial NDI. They provide a convincing proof that mineralcorticoids directly attenuate the expression of aquaporin-2 in the apical membrane of collecting duct, thereby leading to the increase in urine volume in patients with NDI.
To date, familial partial lipodystrophy (FPLD) has been known to consist of seven types, and FPLD type 3 is a rare autosomal dominant genetic disorder caused by mutations of peroxisome proliferator-activated receptor γ gene. In this issue, Dr. Iizaka and colleague report the first pedigree of FPLD 3 in Japanese exemplifying prolonged insulin resistant diabetes mellitus, liver steatosis and hypertriglyceridemia with a relatively low degree of BMI and percentage of body fat. For all endocrinologists, attention should be paid to avoid overlooking lipodystrophy syndromes.
Molecular research on agonists / antagonists / inverse agonists in a variety of G-protein coupled receptors (GPCRs) has long attracted robust attention of endocrinologists. In this issue, Dr. Nagayama and Dr. Nishihara contributes an encyclopedic, well-organized article on the update of antagonists / inverse agonists research around the thyrotropin receptor (TSHR), providing us with promising therapeutic potential for Graves’ hyperthyroidism, non-autoimmune hyperthyroidism, thyroid cancer and resistance to thyroid hormone.
It has long been recognized that uncontrolled high blood pressure, dysmetabolism of glucose and lipids, and sustained inflammation and fibrosis are involved in the pathophysiology and progression of diabetic kidney disease (DKD) in an extremely complexed manner. It is therefore exactly a herculean issue to accurately identify patients with higher risks than we would imagine for end-stage renal diseases (ESRDs). In the October issue, Dr. Xu Ning and colleague provide an attractive review article focusing on potentials of mesenchymal stem cells (MSCs) for the treatment of such an intractable medical condition.
Epigenome-based drugs such as inhibitors against DNA methyltransferases (DNMTs) and histone deacetylase (HDACs) have long been employed for the treatment of a variety of malignancy and pre-cancer status. In this issue, Dr. Rie Hagiwara and colleague provide a convincing data set of in vitro experiments demonstrating a selective HDAC6 inhibitor, tubastatin A substantially suppresses the growth of as well as the ACTH secretion from a murine corticotroph cell line, AtT-20. The present study may open a fresh avenue for brand-new therapeutics in humans on pituitary neuroendocrine tumors including Cushing’s disease.
Science and clinics on phosphate homeostasis are no doubt an authentic, royal road to endocrinology. As most of readers of Endocrine Journal well recognize, basic scientists and endocrinologists in Japan have made a huge contribution to the molecular medicine on fibroblast growth factor 23 (FGF 23) in this academic field. To STATE-OF-THE-ART REVIEW IN ENDOCRINOLOGY in this issue, Dr. Michigami contributes an extensive, well-organized article on the recent research progress in phosphate homeostasis and related disorders with a particular emphasis on FGF 23, providing us with an invaluable perspective for cutting-edge area of bone-mineral endocrinology.
Dynamic remodeling of adipose tissue plays a critical role in the pathophysiology of obesity disease. In this article, Dr. Yutaka Hasegawa elegantly updates the research on the molecular mechanism whereby adipocytes interact with non-adipocytes during the course of adipose dysfunction and fibrosis in obesity. This review does provide us with invaluable perspective for endocrinology-based obesity science.
It has been highlighted that postprandial hyperinsulinemia-associated hypoglycemia sometimes happens in patients with morbid obesity after metabolic surgeries. In the present study, Dr. Yukako Yamamoto and her colleague provide a line of convincing data demonstrating that a 75 g glucose- and high fat-containing cookie meal test is useful in severely obese subjects to precisely evaluate glucose intolerance and postprandial dyslipidemia without occurrence of hyperinsulinemia-associated hypoglycemia. The cookie meal test may open a fresh avenue to conveniently monitor fuel homeostasis in the course of multidisciplinary therapies for obese-diabetic patients.
A variety of factors including dysregulation of renin-angiotensin-aldosterone system in both systemically and locally are well known to affect the progression of diabetic nephropathy (DN).To our surprise, however, the possible association between the plasma renin activity (PRA) and renal outcomes in patients with DN still remains obscure. In the present article, Dr. Kazuyoshi Kuma and colleague elegantly addressed such a unsolved question in a 2 year-prospective study, highlighting that low in PRA is an independent risk for the progression of DN in a Japanese cohort.
X-linked hypophosphatemia (XLH) in known to substantially secrete FGF23, thereby causing renal phosphate loss, chronic hypophosphatemia and a variety of involvement in skeletal system. However, the reality in clinics has not been fully examined. In the present study, via the online questionnaire methods, Ito N et al. comprehensively evaluate the current status and health-related quality of life in patients with XLH living in Japan and Korea, providing us with the latest knowledge and insight into XHL.
Convincing and conveniently-evaluated molecular biomarkers for prediction and assessment of metabolic syndrome are warranted to realize precision health as well as precision medicine in lifestyle-related diseases. In the present study, Yamazaki M and colleague provide intriguing evidence that level of DNA methylation of the gene encoding thioredoxin-interacting protein, a key inhibitor of cellular oxidation, is significantly decreased in peripheral blood cells from subjects with metabolic syndrome. Further extensive studies are strongly expected to see whether such a status of hypomethylation is clinically relevant to the extent of systemic oxidative stress and would be reversible in response to a line of lifestyle modifications or metabolic surgeries.
In this issue, Kamma H and colleague highlight the update of general rules for the description of thyroid cancer proposed by Japanese Society of Thyroid Pathology and Japan Association of Endocrine Surgery. This article is strongly expected to lay a brand-new cornerstone in transferring Japanese diagnostic standard on thyroid cancer for the world.
In this issue, Sugawara L and colleague provide a line of convincing results of genetic analyses on neurophysin II (NPII) in a pedigree of neurohypophyseal diabetes insipidus.