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Purpose: The purpose of this study is to assess the usefulness of liraglutide in elderly patients with type 2 diabetes to prevent progression of dementia. Methods: We retrospectively reviewed 31 outpatients with 65 years of age or older, who have been treated with liraglutide for 6 years (Group G; 12 males/19 females, 73.1 ± 8.6 years-old, HbA1c 7.5 ± 0.4%, 9 patients with cerebrovascular diseases, 8 patients with cardiovascular diseases, 16 patients with insulin therapy). Daily dose of liraglutide was 0.9 mg except 2 patients (0.6 mg). We examined Voxel-based Specific Regional Analysis System for Alzheimer’s Disease (VSRAD) on MRI, max-IMT measured by carotid artery ultrasonography, visceral fat area, concentrations of HbA1c and FPG, serum levels of CRP, HDL/LDL cholesterol, and TG, both before and after the treatment. Age, HbA1c, and VSRAD values-matched 16 patients who were treated with linagliptin were analyzed as a control (Group D). Results: After 6 years, VSRAD was significantly deteriorated in Group D (1.06±0.98→1.39±1.05 (p Conclusion: Liraglutide possibly prevent progression of dementia. The reduction of visceral obesity may contribute to this beneficial effect through anti-arteriosclerosis. Disclosure M. Yoshida: None. A. Yoshida: None. E. Oh: None. N. Yamamoto: None. E. Sasaki: None. S. Yoshida: None. N. Ohsawa: None. M. Sugino: None. I. Koyama: None.

Purpose: The aim of this study was to assess the long-term efficacy of liraglutide on diabetic nephropathy in elderly patients with type 2 diabetes. Methods: Liraglutide was administrated to elderly patients with poorly controlled type 2 diabetes in Aino Hospital. We recruited and retrospectively reviewed 31 patients who were treated with liraglutide for 5 years (Group L: 7 males/24 females, 75.4±8.1 years old of age, 16 with cerebrovascular and 8 patients with cardiovascular diseases at baseline) and 25 patients who were not treated with liraglutide (Group N, 9 males/16 females, 74.6±11.6 years old of age). Daily dose of liraglutide was 0.9mg except 2 patients (0.6 mg). Results: After 5 years of treatment, HbA1c, FPG, and 2h-PPG significantly decreased in both groups (7.5±0.4 to 6.8±0.5 vs. 7.4±0.6 to 6.9±0.4%, 138±19 to 120±11 vs. 132±16 to 113±13, 206±31 to 173±18 vs. 186±23 to 163±18mg/dl, respectively(p60, Group B (n=18): eGFR = 30-60, Group C (n=7): eGFR Conclusion: Liraglutide improved glycemic control, lipid profile and BMI of elderly patients with type 2 diabetes. Liraglutide also demonstrated its beneficial effect on renal function. Disclosure M. Yoshida: None. A. Yoshida: None. E. Oh: None. N. Yamamoto: None. E. Sasaki: None. A. Saeki: None. S. Yoshida: None. T. Kuzuya: None. N. Ohsawa: None. M. Sugino: None.

Purpose: The aim of this study was to assess the efficacy of liraglutide on prevention of dementia in elderly patients with type 2 diabetes (T2DM). Subjects and methods: We studied 34 (male 8/female 26) outpatients with 65 years or older, whose HbA1c was over 7.0% by other antidiabetic treatment. We administrated liraglutide 0.3mg before breakfast for the first week, 0.6mg for the second week, and 0.9mg after the third week. 34 subjects in the liraglutide group (G group) [8 males/ 26 females, 75.7±7.8 years old, HbA1c 7.5 ± 0.38%] were followed-up for 3 years. We examined Voxel-based Specific Regional Analysis System for Alzheimer’s Disease (VSRAD) on MRI, max-IMT measured by carotid artery echo, visceral fat area, HbA1c, FPG, serum HDL/LDL level, and TG, both before and after the treatment.10 patients in the linagliptin group (D group) in which ages, HbA1c, visceral fat, and VSRAD were matched with G group were used as controls. Result: After 3 years, VSRAD was not changed in G group and was significantly deteriorated in D group (G group: 1.22±0.73→1.19±0.73 (NS) vs. G group: 1.36±0.87→1.53±0.99 (p = 0.022)). Max IMT was significantly improved in G group (2.42±1.65→2.14±1.40 (p =0.035) vs. 2.25±1.19→2.19±1.01(NS)). Visceral fat was significantly reduced in G group (137.1±54.0→128.0±59.3 (p Conclusion: Liraglutide improved the glycemic control, lipid profile, and visceral obesity of elderly patients with T2DM for 3 years. In addition, the hippocampal atrophy and arteriosclerosis were not deteriorated, suggesting the possibility of being effective for prevention of dementia. Disclosure M. Yoshida: None. T. Morimoto: None. E. Oh: None. N. Yamamoto: None. K. Nagata: None. A. Saeki: None. E. Sasaki: None. S. Yoshida: None. T. Kuzuya: None. N. Ohsawa: None. M. Sugino: None.

Mutation in the mitochondrial gene at position 3243 was recently identified in a large pedigree of diabetes mellitus and deafness. As the mitochondria play an important role in glucose-stimulated insulin secretion in pancreatic beta-cells, we therefore searched for such mutations to detect a candidate gene for diabetes. We screened 10 diabetic subjects with clinical features suggesting mitochondrial DNA mutations. An adenine to guanine point mutation in tRNA(Lys) in at position 8296 (the 8296 mutation) was newly identified. Subsequently, we screened 1216 diabetic subjects, 44 patients with sensorineural deafness subjects and 300 non-diabetic control subjects for this mutation. We identified the mutation in 11 (0.90%) unrelated diabetic subjects, one (2.3%) patient with deafness and no non-diabetic control subject. Seven of these 12 subjects showed maternal inheritance. Deafness was seen in 7 of 12 probands. Four family pedigrees showed maternal inheritance of diabetes over two or three generations. Subjects carrying the 8296 mutation may develop diabetes and the mutation can explain as high as ca. 1% of the causes of diabetes.

This study attempted to determine whether postprandial hypotension (PPH) is associated with diabetes mellitus by 24-h ambulatory blood pressure monitoring (24-h ABPM) and by monitoring blood pressure during 75-g oral glucose tolerance test (75-g OGTT) in 15 normal subjects and 35 patients with non-insulin-dependent diabetes mellitus. When we defined PPH as a postprandial decrease in systolic blood pressure of greater than 20 mmHg, the incidence of PPH in diabetics was 37% by 24-h ABPM and 20% by 75-g OGTT. The incidence of proliferative retinopathy and proteinuria was greater in diabetics with PPH than in those without PPH. All of the patients with PPH had somatic and autonomic neuropathy. The C-peptide response was lower in diabetics with PPH than in those without PPH. We revealed the presence of PPH in diabetics, and found that PPH was closely related to disease severity, especially diabetic autonomic neuropathy.

We previously showed that diabetes contributes to the development of sclerotic lesions in cerebral arteries. In this study, we attempted to clarify whether differences in heart rate variability in non-hypertensive diabetic patients were dependent on the presence or absence of underlying cerebrovascular disease. Thirty diabetic subjects between 40 and 59 years of age and who had no prior history of hypertension were used in this study. Lacunar lesions (LA) were detected with magnetic resonance imaging and atherosclerotic lesions (AS) were detected using intra- and extracranial magnetic resonance angiography, and by ultrasonographic scanning of the carotid artery. Patients underwent a full clinical laboratory screening and a power spectrum analysis of their heart rate variability. Subjects were divided into two groups: those with and without LA. The low frequency/high frequency ratio (LF/HF ratio) was found to be significantly increased (P

To the Editor: The close relationship between diabetes mellitus and arteriosclerosis of the cerebral arteries has recently been reported. However, in these studies, the subjects included older patients with hypertension, which itself is a significant risk factor for arteriosclerosis of the cerebral arteries.1–3 Thus, previous studies on the effect of diabetes on the development of sclerosis were confounded by hypertension and aging. Therefore, we examined relatively young patients with diabetes mellitus who did not have hypertension in order to clarify the influence of diabetes mellitus itself on the development of sclerosis of the cerebral arteries. The subjects included 30 patients with type 2 diabetes mellitus (DM). The subjects with DM did not have hypertension (systolic blood pressure

We measured pancreatic volume (PV) using helical computed tomography (CT) in 26 patients with type 1 diabetes mellitus (DM), 29 patients with type 2 DM, and 22 healthy individuals. We also evaluated the relationship between PV and the body surface area (BSA), established the pancreatic volume index (PVI) by dividing PV by BSA to correct PV for the body build, and examined its relationships with the duration of illness, serum C-peptide immunoreactivity level (CPR), and serum immunoreactive trypsin level (IRT). BSA and PV were correlated significantly (p

Postprandial hypotension (PPH) is defined as a decrease of systolic blood pressure by more than 20 mmHg after meals. Severe PPH is a troublesome diabetic complication, which has no established means of treatment. We encountered a patient who had diabetes mellitus complicated by severe PPH and attempted to treat this problem using several medications (octreotide, midodrine hydrochloride, and acarbose). A 58-year-old male with diabetic triopathy complained of orthostatic dizziness and vertigo after meals. The blood pressure was monitored for 24 h with an ambulatory blood pressure monitor, revealing that the systolic blood pressure decreased markedly after breakfast and dinner by 45 and 50 mmHg, respectively. PPH was not improved by a subcutaneous injection of octreotide. Administration of midodrine hydrochloride reduced the frequency of hypotensive episodes from twice to once daily, but the magnitude of the postprandial fall in blood pressure was still around 30 mmHg. After the patient started to receive acarbose therapy, the postprandial fall in blood pressure was diminished to 18 mmHg and his symptoms largely disappeared. For the treatment of PPH in diabetic patients, our experience suggests that it may be appropriate to try first on alpha-glucosidase inhibitor like acarbose.

A 44-year-old woman with diabetes mellitus, cardiomyopathy, and a mitochondrial gene mutation, was reported. She was diagnosed as having diabetes at 33 years of age and was treated with insulin. However, she stopped treatment 6 months later and had no medical care until she developed diabetic ketoacidosis at 41 years of age. She had diabetic foot, diabetic retinopathy, and nephropathy with low insulin secretory capacity, leading to insulin treatment. A point mutation of the mitochondrial tRNA(Leu(UUR)) gene was identified in peripheral leukocytes at 43 years of age, and sensorineural hearing impairment was detected at the same time. Her mother also suffered from diabetes mellitus with deafness and her son, who was not diabetic at age 19, had the same mitochondrial DNA (mtDNA) mutation. At 44 years of age, she developed congestive heart failure due to cardiomyopathy, and the same mtDNA mutation was identified in the cardiac muscle. Thus, it is very likely that in this patient, diabetes and cardiomyopathy was caused by the same abnormality, the point mutation of mitochondrial tRNA(Leu(UUR)) gene.

We report a patient, a twin, with diabetes mellitus whose hyperglycemic state fluctuated during the course of the pregnancy and the subsequent delivery. She was diagnosed as having slowly progressive IDDM because of her clinical course and the findings of serum positive ICA/CF, positive HLA-DR4 and disconcordance of diabetes mellitus with her identical twin. Insulin therapy was not initially needed in the first two years because the endogenous insulin secretion was not completely reduced. After two years of insulin therapy the patient became pregnant. Her glycemic control was remarkably improved without changes in dietary intake and insulin dosage. After delivery glycemic control deteriorated after delivery with the occurrence of postpartum thyroiditis. Urinary excretion of CPR was increased during pregnancy but decreased after delivery. ICA/CF in serum were persistently detected in the whole observation period. It seems that the improved glycemic control during pregnancy was caused by the reduction in the autoimmune reaction and the deterioration in glycemic control during the postpartum period was induced by the acceleration of the autoimmune reaction by the same mechanism of postpartum autoimmune thyroiditis.