Search

A study published in the journal Diabetes, Obesity & Metabolism examined the effects of semaglutide injections on treatment satisfaction and eating behavior in Japanese patients with type 2 diabetes mellitus (T2DM). The study found that semaglutide injections increased treatment satisfaction and improved eating behavior in patients with T2DM, particularly those with obesity. The injections also resulted in decreased body weight and HbA1c levels in both groups. However, adverse events were reported, with loss of appetite being the most frequent. The study suggests that semaglutide injections may be a beneficial treatment option for Japanese patients with T2DM and obesity, but further research is needed to confirm these findings. [Extracted from the article]

Aims/Introduction: Recent randomized clinical trials have suggested that sodium–glucose cotransporter 2 inhibitors might reduce cardiovascular events and heart failure, and have renal protective effects. Despite these remarkable benefits, the effects of sodium–glucose cotransporter 2 inhibitors on bone and muscle are unclear. Materials and Methods: A subanalysis of a randomized controlled study was carried out to evaluate the effects of the sodium–glucose cotransporter 2 inhibitor, ipragliflozin, versus metformin on bone and muscle in Japanese patients with type 2 diabetes mellitus (baseline body mass index ≥22 kg/m2 and hemoglobin A1c 7–10%) who were already receiving sitagliptin. These patients were randomly administered ipragliflozin 50 mg or metformin 1,000–1,500 mg daily. The effects of these medications on the bone formation marker, bone alkali phosphatase; the bone resorption marker, tartrate‐resistant acid phosphatase 5b (TRACP‐5b); handgrip strength; abdominal cross‐sectional muscle area; and bone density of the fourth lumbar vertebra were evaluated. Results: After 24 weeks of treatment, the changes in bone density of the fourth lumbar vertebra, handgrip strength and abdominal cross‐sectional muscle area were not significantly different between the two groups. However, TRACP‐5b levels increased in patients treated with ipragliflozin compared with patients treated with metformin (median 11.94 vs −10.30%, P < 0.0001), showing that ipragliflozin can promote bone resorption. Conclusions: There were no adverse effects on bone or muscle when sitagliptin was used in combination with either ipragliflozin or metformin. However, ipragliflozin combination increased the levels of TRACP‐5b. A long‐term study is required to further understand the effects of this TRACP‐5b increase caused by ipragliflozin. [ABSTRACT FROM AUTHOR]

A prospective, multicentre, open‐label, blinded‐endpoint, randomized controlled study was conducted to evaluate the efficacy of treatment with ipragliflozin (sodium‐dependent glucose transporter‐2 inhibitor) versus metformin for visceral fat reduction and glycaemic control among Japanese patients with type 2 diabetes treated with sitagliptin, HbA1c levels of 7%‐10%, and body mass index (BMI) ≥ 22 kg/m2. Patients were randomly assigned (1:1) to receive ipragliflozin 50 mg or metformin 1000‐1500 mg daily. The primary outcome was change in visceral fat area as measured by computed tomography after 24 weeks of therapy. The secondary outcomes were effects on glucose metabolism and lipid metabolism. Mean percentage reduction in visceral fat area was significantly greater in the ipragliflozin group than in the metformin group (−12.06% vs. −3.65%, P = 0.040). Ipragliflozin also significantly reduced BMI, subcutaneous fat area, waist circumference, fasting insulin, and homeostatic model assessment (HOMA)‐resistance, and increased HDL‐cholesterol levels. Metformin significantly reduced HbA1c and LDL‐cholesterol levels and increased HOMA‐beta. There were no severe adverse events. The use of ipragliflozin or metformin in combination with dipeptidyl peptidase‐4 inhibitors, widely used in Japan, may have beneficial effects in ameliorating multiple cardiovascular risk factors. [ABSTRACT FROM AUTHOR]

Cell cycle regulators such as cyclin-dependent kinases (Cdks) and their inhibitors (Ckis) have been reported to be involved in neuronal cell death (NCD) induced by a variety of insults such as ischemia, UV-irradiation, nerve growth factor (NGF)-withdrawal, and anticancer therapeutics. But their precise interactive regulation has still to be unveiled. In the present study, we focused on cell cycle regulators such as Cdk4, p21WAF1 and p53 to clarify their regulatory mechanisms, using NCD induced by doxorubicin (D-NCD) in mouse cerebellar granule neurons as a model. Doxorubicin induced NCD in a dose-dependent manner, a typical feature of apoptosis as determined by TUNEL assay. Doxorubicin increased the protein expression of p53 in time- and dose-dependent manners. The protein expression of p21WAF1, a Cki of Cdk4, was stimulated by doxorubicin at low concentrations, but it disappeared at high concentrations. Doxorubicin activated the kinase activity of Cdk4 without the enhancement of Cdk4 protein. 3-Amino-9-thio(10H)-acridone (3-ATA), the specific inhibitor of Cdk4, prevented D-NCD in a dose-dependent manner. Wortmannin, an inhibitor of ATM (ataxia telangiectasia, mutated) that has high homology with the phosphatidyl-inositol-3-kinase (PI3K) family and has protein kinase activity for the induction of p53 with specificity for serine and threonine residues, inhibited the activation of Cdk4 without the induction of p53 in D-NCD. These data suggest that (1) Cdk4 is one of the essential components for inducing NCD, that (2) p53 may prevent D-NCD through the induction of p21WAF1 at low concentrations of doxorubicin, and that (3) Cdk4 might be activated by the same signal-molecules, like ATM, that are necessary for the activation of p53 in D-NCD. [Copyright &y& Elsevier]

Recently, a combination therapy of several oral agents has been more common for antihyperglycemic therapy and four kinds of combination tablets are available in Japan. Any combination tablet is not allowed for the initial treatment but very useful for a numbers of patients who are already taking two-drug combinations and in stable condition to reduce the number of tablets. Additionally, a combination tablet is also beneficial for patients who are in inadequate glycemic control with a single agent to gain the better glucose lowing effectiveness with a single tablet of dual agents. For a favorable treatment outcome of chronic diseases, it is very important for physicians to enhance drug adherence rate of patients and utilize combination tablets more.

The hyper-responsiveness of plasma cortisol to vasopressin has been reported in patients with ACTH-independent bilateral macronodular adrenocortical hyperplasia (AIMAH) and in certain cases of Cushing's adenomas with overexpression of V1a receptors in the adrenal gland. We previously reported a high prevalence of the adrenal hyper-responsiveness of plasma cortisol to vasopressin (vasopressin responders) in Japanese patients with Cushing's syndrome (CS), in which vasopressin responders had low autonomous cortisol secretion and were diagnosed as having subclinical CS. In the present study, we aimed to evaluate the pathophysiological significance of vasopressin responsiveness in patients with subclinical CS in terms of hormonal secretion and metabolic abnormalities. We compared 14 vasopressin responders and 13 non-responders with subclinical CS, admitted to Chiba University Hospital between 1999 and 2007. Among these patients, the vasopressin responders were found to have lower plasma cortisol levels than non-responders at midnight (P<0.05) and in the morning following overnight dexamethasone suppression at 1 mg (P<0.05). On the other hand, they showed a significantly higher frequency of hypertensive complications than non-responders. In addition, according to 75g-OGTT the vasopressin responders had significantly higher levels of plasma insulin at 60 min than the non-responders, and their cortisol response to vasopressin had a significantly positive association with HOMA-IR (r=0.671, P<0.05). A high expression level of V1a receptor mRNAs was observed in the resected adrenal glands of vasopressin responders with AIMAH and unilateral adenomas. Though vasopressin responders with subclinical CS had lower autonomous cortisol secretion, they had a high prevalence of hypertension, in which insulin resistance was closely correlated with cortisol response to vasopressin.

We report a very rare case of acute pulmonary edema caused by hypoglycemia from insulin overdose during an attempted suicide. A 16-year-old woman with type 1 diabetes was brought to our hospital because of hypoglycemic coma. She exhibited severe hypoxia; upon intubation, bloody froth poured out of the tube. Chest X-ray revealed bilateral infiltrates. Endocrinological data revealed high concentrations of catecholamines. This case indicates that pulmonary edema remains a potential complication of insulin overdose. The possible mechanisms of pulmonary edema associated with hypoglycemia are discussed.

Our hospital is a National General Hospital with 585 beds. We began the visiting care service from 1990 and four visiting staffs are working at present. The number of targets was 69 in 2002 including 32 patients over 70 years old and 20 care-givers over 70 years old. Visiting care has been conducted to a 72-year-old female with diabetes since July 2000. The patient is in bedridden condition and at the beginning of visiting, she was taking oral medication but the condition was worsen by poor glycemic control and changed to insulin injection from June 2002 after admission to the hospital repeatedly. The patient undergoes the measurement of blood sugar daily and takes meals with 1,200 to 1,400 kcal prepared by her husband. The care-giver is a 71-year-old husband. He was an "all-work, no-play" type of person and had never done the housework, but he started to manage both housework and nursing because of bedridden of his wife. He is a reticent theorist, hates illogical behavior, and does not swayed by other opinions. He has accepted the things which need new knowledge and techniques such as measurement of blood glucose and insulin injection. However, for meals, he only bought side dishes and placed them. Care such as keeping the patient clean was in a same state. The patient consulted and admission to the hospital repeatedly because conditions were not stable. Visiting nurse supported daily life of patient and care-giver especially in nutrition instruction to continue home life. As the result, attitude and behavior toward nursing of care-giver were changed and the patient could continue home life. Therefore we reported here.