Aspartame is a low calorie sugar that is widely used in artificial sweeteners. Although different studies indicated associated health symptoms to it, it continues to be controversial. Studies have also shown consumption of aspartame caused neurological deficits and mitochondrial mediated activation of apoptosis was observed as a long-term effect of aspartame in rat brain. In this study, the biochemical responses of distal tubular kidney cells upon short-term exposure to aspartame were measured. MDCK Type II (kidney) cells were exposed to 50 µg/ml to 250 µg/ml aspartame for 30 mins. Mitochondrial linked biochemical responses such as oxidative stress and energy production was measured. Overall increase in dehydrogenase activity together with increased production of ATP was observed. This was accompanied by an overall increase in mitochondria derived oxidative stress. However, mitochondrial membrane potential and cellular NAD/NADH ratio in the aspartame exposed cells remained unchanged. These results indicate that while aspartame did not cause significant changes in the mitochondrial activity, the elevated activity of the mitochondria shown through the increase in ATP production and oxidative stress indicate the involvement of the mitochondria in aspartame-mediated cellular response. More studies would need to be done to clarify the mechanism by which aspartame increases oxidative stress via the mitochondria.
{"title":"Mitochondria-Derived Oxidative Stress Associated with Aspartame Effect on Kidney Cells","authors":"A. Maria, A. Maryam, Shoba Va","doi":"10.16966/2380-548x.161","DOIUrl":"https://doi.org/10.16966/2380-548x.161","url":null,"abstract":"Aspartame is a low calorie sugar that is widely used in artificial sweeteners. Although different studies indicated associated health symptoms to it, it continues to be controversial. Studies have also shown consumption of aspartame caused neurological deficits and mitochondrial mediated activation of apoptosis was observed as a long-term effect of aspartame in rat brain. In this study, the biochemical responses of distal tubular kidney cells upon short-term exposure to aspartame were measured. MDCK Type II (kidney) cells were exposed to 50 µg/ml to 250 µg/ml aspartame for 30 mins. Mitochondrial linked biochemical responses such as oxidative stress and energy production was measured. Overall increase in dehydrogenase activity together with increased production of ATP was observed. This was accompanied by an overall increase in mitochondria derived oxidative stress. However, mitochondrial membrane potential and cellular NAD/NADH ratio in the aspartame exposed cells remained unchanged. These results indicate that while aspartame did not cause significant changes in the mitochondrial activity, the elevated activity of the mitochondria shown through the increase in ATP production and oxidative stress indicate the involvement of the mitochondria in aspartame-mediated cellular response. More studies would need to be done to clarify the mechanism by which aspartame increases oxidative stress via the mitochondria.","PeriodicalId":73446,"journal":{"name":"International journal of endocrinology and metabolic disorders","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67390642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: To report an episode of diabetic ketoacidosis and acute kidney failure in a patient with type 2 diabetes (T2DM) recently initiated a sodiumglucose co-transporter 2 inhibitor (SGLT-2i) and a DDPP-4 inhibitor (DDP-4i). Methods: We describe the clinical presentation, laboratory data and management of an elderly T2DM patient with diabetic ketoacidosis. Results: A 80 year-old T2DM female presented with, fatigue, nausea, recurrent vomiting, muscle pain, malaise and shortness of breath three weeks after initiation of dapagliflozin 5 mg and sitagliptin 100 mg. On admission to the emergency department, the patient was hypotensive, and rapidly became comatose. The glucose concentration was 398 mg/dL, Na 135 mmol/L, K 4.1 mmol/L, pH 6.8, and bicarbonate 1.8 mmol/L, blood urea nitrogen 22.8 mg/dL, creatinine 0.96 mg/dL, beta-hydroxybutirate 3.2 mmol/L and lactate 1.1 mmol/L. The estimated osmolality was 300.25 mOsm/L and the anion gap 26.7 mEq/L. C-reactive protein was <2.5 mg/L. Urine sample was normal and urine culture was negative. Hemoglobin was 12.6 g/dL; leucocyte count was 21.0 × 103 μL and platelet count 253 × 103 μL. Two days after hospitalisation the patient developed an acute kidney failure and anemia. The patient was treated with balanced electrolyte solutions, continuous insulin infusion and IV antibiotics and dapagliflozin was discontinued. Diabetic ketoacidosis resolved in 48 hours and the acute kidney failure in 6 days. The patient was discharged 10 days after admission with a basal bolus regimen with insulin analogues. Conclusions: This elderly patient with long lasting type 2 diabetes treated with SGLT-2i developed diabetic ketoacidosis and acute kidney failure. This complication occurred associated with dietary derangements and lack of insulin treatment. Each medication change needs a very clear indication; otherwise it adds more risk to the patient than benefit. When prescribing SGLT2i in diabetics, physician must assure diabetes education, an adequate insulin provision and strict monitoring of glucose and urine ketones.
{"title":"Diabetic Ketoacidosis Linked with Sodium Glucose Co-Transporter 2 Inhibitors in an Elderly Patient with Type 2 Diabetes","authors":"Jiménez-Montero Jg","doi":"10.16966/2380-548X.154","DOIUrl":"https://doi.org/10.16966/2380-548X.154","url":null,"abstract":"Objective: To report an episode of diabetic ketoacidosis and acute kidney failure in a patient with type 2 diabetes (T2DM) recently initiated a sodiumglucose co-transporter 2 inhibitor (SGLT-2i) and a DDPP-4 inhibitor (DDP-4i). Methods: We describe the clinical presentation, laboratory data and management of an elderly T2DM patient with diabetic ketoacidosis. Results: A 80 year-old T2DM female presented with, fatigue, nausea, recurrent vomiting, muscle pain, malaise and shortness of breath three weeks after initiation of dapagliflozin 5 mg and sitagliptin 100 mg. On admission to the emergency department, the patient was hypotensive, and rapidly became comatose. The glucose concentration was 398 mg/dL, Na 135 mmol/L, K 4.1 mmol/L, pH 6.8, and bicarbonate 1.8 mmol/L, blood urea nitrogen 22.8 mg/dL, creatinine 0.96 mg/dL, beta-hydroxybutirate 3.2 mmol/L and lactate 1.1 mmol/L. The estimated osmolality was 300.25 mOsm/L and the anion gap 26.7 mEq/L. C-reactive protein was <2.5 mg/L. Urine sample was normal and urine culture was negative. Hemoglobin was 12.6 g/dL; leucocyte count was 21.0 × 103 μL and platelet count 253 × 103 μL. Two days after hospitalisation the patient developed an acute kidney failure and anemia. The patient was treated with balanced electrolyte solutions, continuous insulin infusion and IV antibiotics and dapagliflozin was discontinued. Diabetic ketoacidosis resolved in 48 hours and the acute kidney failure in 6 days. The patient was discharged 10 days after admission with a basal bolus regimen with insulin analogues. Conclusions: This elderly patient with long lasting type 2 diabetes treated with SGLT-2i developed diabetic ketoacidosis and acute kidney failure. This complication occurred associated with dietary derangements and lack of insulin treatment. Each medication change needs a very clear indication; otherwise it adds more risk to the patient than benefit. When prescribing SGLT2i in diabetics, physician must assure diabetes education, an adequate insulin provision and strict monitoring of glucose and urine ketones.","PeriodicalId":73446,"journal":{"name":"International journal of endocrinology and metabolic disorders","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67390401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A Rare Case of a Giant Adrenal Incidentaloma in 78 Year Old: Incidence, Radiologic and Management Issues of Adrenal Myelolipoma","authors":"Tan Elq, Tan Gh","doi":"10.16966/2380-548x.162","DOIUrl":"https://doi.org/10.16966/2380-548x.162","url":null,"abstract":"","PeriodicalId":73446,"journal":{"name":"International journal of endocrinology and metabolic disorders","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67390926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Normotensive, Normokalemic Hyperaldosteronemia of a Grown-up Woman Diagnosed as Salt-Losing 21-Hydroxylase Deficiency in Neonatal Period","authors":"Yamamoto T","doi":"10.16966/2380-548x.153","DOIUrl":"https://doi.org/10.16966/2380-548x.153","url":null,"abstract":"","PeriodicalId":73446,"journal":{"name":"International journal of endocrinology and metabolic disorders","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67390357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Calcium loss by lactation does not cause hypocalcemia unless mothers have subclinical hypoparathyroidism. Case report: A 32-year-old woman was an inhabitant of an island located in the south-western region of Japan. She delivered her second boy by Caesarian section in 37th week of gestation in a hospital in the mainland. She began milking the breasts 6 to 7 times a day, yielding ca. 200 ml each times, on 4th post-operative (henceforth, PO day). She left her baby in the hospital and returned her home island on the 7th PO day. Then, she continued milking the breasts daily and shipped milk to the hospital for her baby. On the 13th PO day, she noticed paresthesia around the mouth and in both hands. Following day, she was admitted in author’s hospital for hypocalcemic crisis with intermittent carpopedal spasm and opisthotonos on rare occasions. The initial blood study revealed serum albumin 3.4 g/dl, calcium 4.6 mg/dl (reference range, 8.6-10.2), inorganic phosphate 1.6 mg/ dl (reference range, 1.7-2.6). She was given i.v. injections of 8.5% calcium gluconate, 10 ml and 20 ml successively, which was followed by continuous i.v. infusion of calcium-enriched saline until the 15th PO day. Serum calcium normalized after cessation of milking. Serum intact parathyroid hormone level was 153 pg/ml (reference range, 10-65) at the time of the admission. Conclusion: The amount of milk mother produces is determined by baby’s sucking. When mother is separated from her baby, she might milk the breasts more than the baby’s need. Excessive milking has conceivably precipitated hypo-calcemic crisis in the present patient.
{"title":"Hypocalcemic Crisis Induced by Excessive Milking Running Title: Milking-Induced Hypocalcemic Crisis","authors":"T. Yamamoto, I. Sy","doi":"10.16966/2380-548x.159","DOIUrl":"https://doi.org/10.16966/2380-548x.159","url":null,"abstract":"Background: Calcium loss by lactation does not cause hypocalcemia unless mothers have subclinical hypoparathyroidism. Case report: A 32-year-old woman was an inhabitant of an island located in the south-western region of Japan. She delivered her second boy by Caesarian section in 37th week of gestation in a hospital in the mainland. She began milking the breasts 6 to 7 times a day, yielding ca. 200 ml each times, on 4th post-operative (henceforth, PO day). She left her baby in the hospital and returned her home island on the 7th PO day. Then, she continued milking the breasts daily and shipped milk to the hospital for her baby. On the 13th PO day, she noticed paresthesia around the mouth and in both hands. Following day, she was admitted in author’s hospital for hypocalcemic crisis with intermittent carpopedal spasm and opisthotonos on rare occasions. The initial blood study revealed serum albumin 3.4 g/dl, calcium 4.6 mg/dl (reference range, 8.6-10.2), inorganic phosphate 1.6 mg/ dl (reference range, 1.7-2.6). She was given i.v. injections of 8.5% calcium gluconate, 10 ml and 20 ml successively, which was followed by continuous i.v. infusion of calcium-enriched saline until the 15th PO day. Serum calcium normalized after cessation of milking. Serum intact parathyroid hormone level was 153 pg/ml (reference range, 10-65) at the time of the admission. Conclusion: The amount of milk mother produces is determined by baby’s sucking. When mother is separated from her baby, she might milk the breasts more than the baby’s need. Excessive milking has conceivably precipitated hypo-calcemic crisis in the present patient.","PeriodicalId":73446,"journal":{"name":"International journal of endocrinology and metabolic disorders","volume":"294 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67390719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Primary Aldosteronism is the single most common cause of secondary hypertension and is associated with increased target organ injury. The Endocrine Society has recently released the updated Clinical Practice Guideline for Primary Aldosteronism entitled "The Management of Primary Aldosteronism: Case Detection, Diagnosis, and Treatment: An Endocrine Society Clinical Practice Guideline". We review the updated Clinical Practice Guideline, highlighting the new recommendations and the implications that they may have in clinical practice. The recognition by the Endocrine Society's Task Force that Primary Aldosteronism is a public health issue and that the population at risk for screening should be significantly expanded will surely have an impact in the clinical practice which hopefully will translate in better detection, diagnosis and treatment of patients with Primary Aldosteronism.
{"title":"Clinical Practice Guideline for Management of Primary Aldosteronism: What is New in the 2016 Update?","authors":"Damian G Romero, Licy L Yanes Cardozo","doi":"10.16966/2380-548X.129","DOIUrl":"https://doi.org/10.16966/2380-548X.129","url":null,"abstract":"<p><p>Primary Aldosteronism is the single most common cause of secondary hypertension and is associated with increased target organ injury. The Endocrine Society has recently released the updated Clinical Practice Guideline for Primary Aldosteronism entitled \"The Management of Primary Aldosteronism: Case Detection, Diagnosis, and Treatment: An Endocrine Society Clinical Practice Guideline\". We review the updated Clinical Practice Guideline, highlighting the new recommendations and the implications that they may have in clinical practice. The recognition by the Endocrine Society's Task Force that Primary Aldosteronism is a public health issue and that the population at risk for screening should be significantly expanded will surely have an impact in the clinical practice which hopefully will translate in better detection, diagnosis and treatment of patients with Primary Aldosteronism.</p>","PeriodicalId":73446,"journal":{"name":"International journal of endocrinology and metabolic disorders","volume":"2 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5175479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9709634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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