Volume 1 Issue 2
Mini Review Location of Anterior Pituitary Gland Tissue is interrelated with Sella Turcica Morphology in Human Fetuses - Review and Perspective
This mini review is based on immunohistochemical studies on the human pituitary gland during the last 25 years. The normal development of the pituitary gland and its supporting sella turcica is presented. Further-more focus is on pathological development, demonstrating ectopic adeno-pituitary gland tissue and abnormal sella turcica morphology. It is highlighted how the sella turcica morphology can predict abnormal formation and ectopic locations of the anterior pituitary gland tissue.
Cite this Article: Kjaer I. Location of Anterior Pituitary Gland Tissue is interrelated with Sella Turcica Morphology in Human Fetuses - Review and Perspective. Int J Clin Endocrinol. 2017;1(2): 059-062.
Published: 31 December 2017
There is evidence that conditioned hunger promotes fattening/diabetes that cannot be actually contrasted if conditioned intake is scientifically accepted as normal. The adoption of a meal pattern based on demand is easy in the first days of life and effective in suppressing or reducing conditioned intake. The National Child Study might compare the prevalence of diseases development between rearing children by conditioned intake versus rearing by demand. In the case of a failure, the Study shall show the role of conditioned eating on fattening diabetes.
Cite this Article: Ciampolini M. Feeding either Conditioned or by Demand. Int J Clin Endocrinol. 2017;1(2): 056-058.
Published: 27 November 2017
Thyroid Hormones (THs) regulate the development of all biological systems, particularly CNS [1-30], neuronal excitability and the ionic gradient [6,8]. The fetal hypothyroidism diminished the levels of nucleotides, ATPases (Na+, K+-ATPase, Ca2+-ATPase and Mg2+-ATPase) activities, and total adenylate; however, the adenylate energy charges displayed a tendency to an increase in cerebrum and cerebellum at gestation days 15 and 20 . The synthesis of ATP delays considerably during hypothyroidism state  and changed the hydrolysis of adenine nucleotide in synaptosomes from hippocampus and cerebral cortex of rats .
Cite this Article: Ahmed RG. Thyroid Diseases and Developmental Adenosinergic Imbalance. Int J Clin Endocrinol. 2017;1(2): 053-055.
Published: 08 September 2017
Case Report Euglycemic Diabetic Ketoacidosis Complicating use of an SGLT-2 Inhibitor in a Patient with Undiagnosed Type 1 Diabetes Mellitus: A Case Report
Shahzeena Hafeez* and Israel Orija
Introduction: The use of sodium-glucose cotransporter 2 (SGLT-2) inhibitors have recently increased in patients with Diabetes Mellitus Type 2 (DM2). However their off label use in patients with Diabetes Mellitus Type 1 (DM1) is gradually increasing and thus exposing these patients to an increased risk of Euglycemic Diabetic Ketoacidosis (EuDKA). The aim of this case report is to emphasize the challenges encountered while treating a patient with EuDKA who was on an SGLT-2 inhibitor for presumptive DM2 and hope that such a complication can be avoided in the future.
Case report: We report a patient with DM2, being treated with Glyburide, Glucophage and recently added Canagliflozin, with clinical findings suggestive of diabetic ketoacidosis. Despite appropriate treatment and return of her blood glucose to normal, her anion gap remained persistently elevated, with low serum bicarbonate and positive urinary ketones and glucose, thus confirming the diagnosis of EuDKA that required prolonged intravenous insulin therapy.
Conclusion: This case reinforces the fact that SGLT-2 inhibitors should be withheld or used with extreme caution in treating DM1 patients.
Cite this Article: Hafeez S, Orija I. Euglycemic Diabetic Ketoacidosis Complicating use of an SGLT-2 Inhibitor in a Patient with Undiagnosed Type 1 Diabetes Mellitus: a Case Report. Int J Clin Endocrinol. 2017;1(2): 049-052.
Published: 01 September 2017
Maria Sorrentino* and Giovanni Ragozzino
The response in terms of eating habits is therefore that, in times of abundance, the introduction of food should be reduced and energy consumption should increase, while the opposite would occur in times of famine. In order to maintain the energy homeostasis, during the evolutionary phases of eating habits, complex regulatory mechanisms (hunger/ satiety system) have established, involving central (hypothalamus) and peripheral (gastrointestinal tract, adipose tissue) structures. Energy balance stems from the relationship between energy expenditure and energy availability. It is managed by the endocrine-metabolic and hunger/ satiety system, mainly ruled by the hypothalamic centers at the encephalic level. The hypothalamus receives impulses from periphery as metabolic and endocrine nervous stimuli, informing the central nervous system on the nutritional status of the body, and through which food intake is regulated. The senses involved in food contact - taste, smell, sight, tactile features and palatability - represent the encephalic responses affecting eating behaviour. Palatability depends not only on food organoleptic characteristics but also on emotional state as well as cultural and environmental factors. This is because the secondary taste area communicates with cortical areas expressing emotions and memory, and with subcortical structures regulating hunger and satiety. Often, however, environmental influences interact with physiological control and stimulate consumption independently of satiety or inhibit it regardless of hunger. The hedonic properties of food can in fact stimulate its consumption even when energy needs have been met, thus contributing to increased weight and obesity. This review aims to describe the main mechanisms and mediators involved in maintaining the energy homeostasis and regulating food intake, the intracellular actions with which these mediators influence food intake and metabolism, as well as the complex system of interactions between the central nervous system and periphery, highlighting the powerful enhancing effects of food in the central reward system.
Cite this Article: Sorrentino M, Ragozzino G. The Regulation of Food Intake: the Brain-Endocrine Network. Int J Clin Endocrinol. 2017;1(2): 041-048.
Published: 29 August 2017
Ram B. Jain*
Data from National Health and Nutrition Examination Survey for those aged >= 12 years for 2007-2012 were used to evaluate associations between the levels of urine and blood cadmium and thyroid hormones: Thyroid Stimulating Hormone (TSH), Free and Total Triiodothyronine (FT3, TT3), Free and Total Thyroxine (FT4, TT4), and Thyroglobulin (TGN). Separate regression models for iodine deficient males, iodine replete males, iodine deficient females, and iodine replete females were fitted. Total sample sizes used to analyze blood cadmium data were 1293, 3367, 1455, and 2586 for iodine deficient male, iodine replete males, iodine deficient females, and iodine replete females respectively. Total sample sizes used to analyze urine cadmium data were 444, 1122, 482, and 892 for iodine deficient male, iodine replete males, iodine deficient females, and iodine replete females respectively. For iodine deficient males, for one decile increase in the levels of blood cadmium, the adjusted levels of TT3 and TT4 increased by 0.007 ng/dL and 0.007 μg/mL respectively. For iodine replete males, for a 10% increase in the levels of blood cadmium, levels of TGN increased by 0.643%. For iodine deficient females, for one decile increase in the levels of blood cadmium, the levels of FT3 increased by 0.008 pg/mL and the levels of TT3 decreased by 0.012 ng/dL. For iodine replete females, for one decile increase in the levels of blood cadmium, the levels of FT3 increased by 0.006 pg/mL and the levels of TT3 decreased by 0.007 ng/dL. Blood cadmium levels did not affect the levels of TSH. The levels of urine cadmium were not found to affect the levels of any thyroid hormone.
Keywords: Thyroid hormones; Cadmium; FT4; TT3; TT4; TSH
Cite this Article: Jain RB. Associations between Thyroid Function and Blood and Urine Cadmium. Int J Clin Endocrinol. 2017;1(1): 033-040.
Published: 23 August 2017
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