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Hiromu Nakajima

Publications and source records attributed to Hiromu Nakajima.

16 recordsLinked to original sources
PubMed2006

Ghrelin reduction after esophageal substitution and its correlation to postoperative body weight loss in esophageal cancer patients.

BACKGROUND: Body weight loss is observed commonly after esophagectomy with gastric tube reconstruction in thoracic esophageal cancer patients. The functional and anatomical alteration of the stomach by this surgery should affect ghrelin secretion, a novel gastric hormone that upregulates body weight through appetite control and metabolic reaction. METHODS: Early-phase postoperative alteration of serum ghrelin was measured before and at day 3 and day 7 after surgery in 9 patients. With 26 other patients, who had previously undergone surgery from 3 months to 67 months (mean, 25 months) before the present study period, the late-phase postoperative alteration of serum ghrelin was investigated along with postoperative body weight loss and serum leptin. RESULTS: Serum ghrelin concentration, which was equivalent to the control group before surgery (88.6 fmol/mL vs 97.5 fmol/mL) significantly decreased by half at 3 and 7 days after surgery. Thereafter, the serum ghrelin decline continued in the outpatients within 1 year after surgery (58.8 fmol/mL), while it was marginal in those from 1 to 3 years after surgery (77.2 fmol/mL). Serum ghrelin was significantly higher than the control after 3 years (185.1 fmol/mL). Thus, a significant positive correlation was observed between ghrelin and time after surgery (P < .0001). Postoperative body weight loss was significant, averaged as DeltaBMI - 2.7 in the outpatients (P < .0001). Until 3 years after surgery, a significant correlation between ghrelin and postoperative body weight loss was observed (P = .0152), with those having higher serum ghrelin showing less body weight loss. Serum leptin correlated well with body weight (P = .0144), but not with postoperative time, the degree of body weight loss, or serum ghrelin concentration. CONCLUSION: Gastric tube replacement for esophagectomy resulted in temporary reduction of ghrelin production, which is associated with body weight loss after surgery. The decline of ghrelin may play some role in the serious body weight loss after esophagectomy, thus encouraging clinical application of exogenous recombinant ghrelin for these patients.

Aged↗
PubMed2005

Postoperative ghrelin levels and delayed recovery from body weight loss after distal or total gastrectomy.

BACKGROUND: Body weight loss is a common but one of the most serious sequelae after gastrectomy. Ghrelin, a novel gastric hormone that up-regulates body weight through appetite control and metabolic reaction, seems to be affected by gastric surgery. PATIENTS AND METHODS: Early postoperative alteration of serum ghrelin was evaluated at days 3 and 7 after gastrectomy for 13 hospital patients. In 64 outpatients who had previously undergone total gastrectomy (TG: 26 patients) or distal gastrectomy (DG: 38 patients) 4.6 months to 136 months (average, 41 months) earlier, the association between their serum ghrelin and leptin levels and postoperative body weight was investigated. RESULTS: Serum ghrelin declined immediately and greatly after TG to 12% of the preoperative level (day 3 and day 7), whereas the decline was less significant after DG at 39% (day 3) and 56% (day 7). In outpatients, serum ghrelin after TG was very low compared with the control (18.6 fmol/mL versus 92.1 fmol/mL, P<0.0001), irrespective of the period after surgery, whereas the level after DG recovered and was equivalent to the control (73.4 fmol/mL, P=0.355). Body weight loss was more apparent in TG patients than in DG patients, showing postoperative reduction of body mass index (DeltaBMI) -3.940 versus -1.949 (P<0.0001). Serum leptin concentration, reflecting the systemic fat volume, significantly correlated with BMI in both TG and DG patients, and tended to be lower in TG patients than in DG patients (800 pg/mL versus 1158 pg/mL, P=0.236). CONCLUSION: Persistent decline of serum ghrelin and body weight was observed commonly after total gastrectomy. Further study is needed as to whether or not ghrelin administration can improve the body weight level for these patients.

Aged↗
PubMed2004

Cloning and reporter analysis of human mitochondrial phosphoenolpyruvate carboxykinase gene promoter.

Phosphoenolpyruvate carboxykinase (PEPCK) is one of the key regulatory enzymes in gluconeogenesis. In human liver, PEPCK is about equally distributed in both cytosol (PEPCK-1) and mitochondria (PEPCK-2). The human pepck2 gene and cDNA have been reported, but the cloning of the promoter region of the pepck2 gene has not been elucidated yet. We isolated and characterized human genomic P1-artificial chromosome (PAC) clones carrying the human pepck2 gene promoter. The oligocapping method revealed that the transcriptional start point (tsp) of the human pepck2 gene is located at 97 bp upstream of the first adenine residue of the translation start site. We also determined the nucleotide sequence to 1819 bp upstream of tsp. Sequence analysis of this region revealed that it contained several potential regulatory elements, including five GC boxes and three CCAAT boxes. Reporter analysis using transient transfection with firefly luciferase synthetic gene indicated 5' flanking region up to 822 bp, and 317 bp upstream of tsp had transcriptional activity. These results suggest that these regions of the human pepck2 gene play an important role for its expression.

Base Sequence↗
PubMed2004

Novel testis- and embryo-specific isoforms of the phosphofructokinase-1 muscle type gene.

We have identified novel transcriptional isoforms of the human and mouse genes encoding muscle type phosphofructokinase-1 (PFK-M). These isoforms are expressed specifically in the testis and in the mid-gestation embryo, and have been termed TE-PFK-M (testis- and embryo-specific PFK-M). The 5'UTR of TE-PFK-M is composed of three newly identified exons that lie much farther upstream of the PFK-M coding region than the previously characterized 5'UTR. In addition, this upstream region encodes a series of small polyadenylated transcripts, some of which share the same exons found in the 5'UTR of TE-PFK-M, and which may play some role in regulating TE-PFK-M expression. These findings indicate an even more complex level of control of PFK-M expression than previously thought.

Animals↗
PubMed2004

Intermittent and recurrent hepatomegaly due to glycogen storage in a patient with type 1 diabetes: genetic analysis of the liver glycogen phosphorylase gene (PYGL).

We report a 19-year-old woman who had a history of type 1 diabetes with recurrent glycogen accumulation in the liver. During her infantile period she presented with no hepatomegaly nor growth retardation. On admission she was diagnosed with diabetic ketoacidosis (DKA). She also had hepatomegaly and elevated transaminase levels, but these abnormalities had resolved after administration of insulin. However, 4 weeks after DKA marked hepatomegaly and elevated transaminases were reappeared with simultaneous hypoglycemia which suggested an impaired glycogenolysis in the extraordinary conditions. We supposed the partial deficiency of liver glycogen phosphorylase activity in this patient and analyzed the liver glycogen phosphorylase gene (PYGL). Deduced amino acid sequence of the PYGL in this patient was completely identical to that reported by Burwinkel et al. (Y15233), however, the nucleotide sequence of PYGL cDNA was heterozygous for substitutions at positions Asp339 (GAT to GAC) on exon 9 and Ala703 (GCT to GCC on exon 17, respectively. These SNPs were also screened in 51 Japanese normal subjects by PCR-based direct sequencing or PCR-RFLP method. The same genotype observed in this patient was detected in 2 of 51(3.9%) normal subjects. These results suggest that the structure of PYGL coding sequence in this patient is unlikely to account for her excessive liver glycogen accumulation. Further studies including genetic analysis on the promoter region of the gene are necessary to clarify the etiology of susceptibility to excessive liver glycogen storage in patients with type 1 diabetes.

Adult↗
PubMed2004

Randomized, controlled trial of secondary prevention of coronary sclerosis in normocholesterolemic patients using pravastatin: final 5-year angiographic follow-up of the Prevention of Coronary Sclerosis (PCS) study.

BACKGROUND: The potential benefit of cholesterol-lowering therapy for normocholesterolemic patients with coronary artery disease (CAD) has not been clarified. The Prevention of Coronary Sclerosis (PCS) Study was designed to evaluate the effect of pravastatin on secondary prevention of progression of CAD in normocholesterolemic patients for a period of 5 years. METHODS: A total of 329 patients with CAD were enrolled. Normocholesterolemic patients were defined by a serum total cholesterol (TC) level of 180-219 mg/dl. Patients in this group were randomized into pravastatin and dietary control groups. Patients whose serum TC level fell outside the normal range were divided into a high-cholesterol reference group (TC > or = 220 mg/dl) and a low-cholesterol reference group (TC < 180 mg/dl). Patients in the pravastatin and high-cholesterol groups received pravastatin 10 mg/day. Coronary angiography was performed at baseline, 2 years, and 5 years and analyzed by quantitative coronary arteriography. Angiographic coronary progression was evaluated by minimum obstruction diameter (MOD) and mean segment diameter (MSD). RESULTS: At 5 years, change in MOD was significantly (change, P=0.033; change/years, P=0.032) less in the pravastatin group (-0.04 +/- 0.17 mm) than in the dietary control group (-0.16 +/- 0.27 mm). Although a similar trend was observed in the MSD results, the differences were not significant. CONCLUSION: Long-term angiographic data show that cholesterol-lowering therapy by pravastatin prevents progression of coronary atherosclerosis in normocholesterolemic patients with CAD.

Adult↗
PubMed2004

[Uric acid].

Explore the source record for details and available documents.

Humans↗
PubMed2003

[Management of hyperuricemia in occupational health: with reference to "guidelines for the management of hyperuricemia and gout"].

In 1996, the need for the clinical guidelines for the management of hyperuricemia and gout was proposed of the consensus conference held at the 29th annual meeting of the Japanese Society of Purine and Pyrimidine Metabolism (president Yuji Matsuzawa). At the consensus conference, the following announcement was made. 1. Because the majority of patients with hyperuricemia are in the condition of multiple risk factor clustering syndrome, hyperuricemia per se should be counted as one of the typical lifestyle related diseases. 2. Medical management should be directed independently for the treatment of gouty arthritis and for control of the serum uric acid level. 3. The serum uric acid level should be taken into account as a possible cardiovascular risk factor. 4. Urine alkalization should be started if there is no symptom indicating hyperuricemia for the prophylaxis of urinary stones and renal dysfunction. 5. All the medical management should be considered under the consensus of the many expert physicians dealing with hyperuricemia and gout. This principal announcement was made by the consensus conference and the simple management recommendation of a 6-7-8 rule was proposed through the consensus of expert physicians. Recently, a guideline committee was organized in the Japanese Society of Gout and Nucleic Acid Metabolism (previous by the Japanese Society of Purine and Pyrimidine Metabolism) and the Guidelines for the Management of Hyperuricemia and Gout were prereleased in February and published in August 2002. In the new guidelines, the above policy was introduced and evidence was collected to give the guidelines contemporary clinical usefulness and value. It will help in the proper management of hyperuricemia in apparently healthy persons in occupational health, having multiple risk factors.

Arteriosclerosis↗
PubMed2002

Metabolic consequence of long-term exposure of pancreatic beta cells to free fatty acid with special reference to glucose insensitivity.

Long-term exposure of the pancreatic beta cells to free fatty acid (FFA) reportedly inhibits glucose-stimulated insulin secretion. We here studied the impact of FFA on glucose and lipid metabolism in pancreatic beta cells with special reference to insulin secretion. Pancreatic beta-cell line MIN6 was exposed to various concentrations of palmitate for 3 days. Glucose-stimulated insulin secretion and insulin content were decreased corresponding to the concentration of the palmitate exposed. Glycolytic flux and ATP synthesis was unchanged, but pyruvate-stimulated change in NAD(P)H concentration was decreased. Pyruvate carboxylase was decreased at the protein level, which was restored by the removal of palmitate or the inhibition of beta-oxidation. Intracellular content of triglyceride and FFA were elevated, beta-oxidation was increased, and de novo lipogenesis from glucose was decreased. NADPH content and citrate output into the medium, which reflected pyruvate malate shuttle flux, were decreased, but malic enzyme activity was unaffected. The malic enzyme inhibitor alone inhibited insulin response to glucose. In conclusion, long-term exposure of FFA to beta cells inhibits glucose-stimulated insulin secretion via the decreased NADPH contents due to the inhibition of pyruvate carboxylase and malate pyruvate shuttle flux.

Animals↗
PubMed2002

Phosphofructokinase deficiency; past, present and future.

Phosphofructokinase deficiency (Tarui disease, glycogen storage disease VII, GSD VII) stands out among all the GSDs. PFK deficiency was the first recognized disorder that directly affects glycolysis. Ever since the discovery of the disease in 1965, a wide range of biochemical, physiological and molecular studies of the disorder have greatly expanded our understanding of the function of normal muscle, general control of glycolysis and glycogen metabolism. The studies of PFK deficiency vastly enriched the field of glycogen storage diseases, as well as the field of metabolic and neuromuscular disorders. This article cites a historical overview of this clinical entity and the progress that has been made in molecular genetic area. We will also present the results of a search in-silico, which allowed us to identify a previously unknown sequence of the human platelet PFK gene (PFK-P). In addition, we will describe phylogenetic analysis of evolution of PFK genes.

Adolescent↗