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Biomedical subjects

M Narimiya

Publications and source records attributed to M Narimiya.

15 recordsLinked to original sources
PubMed2000

A diabetic patient with scrotal subcutaneous abscess.

A 51-year-old type 2 diabetic patient with a scrotal subcutaneous abscess is reported. He was diagnosed as having diabetes mellitus five years earlier. He had left scrotal swelling and pain with granulocytosis, elevated C-reactive protein and hyperglycemia. He was successfully treated with incision and drainage (Streptococcus agalactiae was identified in the pus), debridement, antibiotics, immunoglobulin and insulin. This case resembled Fournier's gangrene, an infective necrotizing fasciitis of the perineal, genital or perianal regions. Diabetes mellitus is a basic disorder often associated with Fournier's gangrene. Scrotal subcutaneous abscess should be prevented from progressing to Fournier's gangrene with early and appropriate treatment.

Abscess↗
PubMed1996

[Diet therapy].

The effect of diet therapy on borderline type was discussed here. First the effect of calorie restriction on preventing the development of diabetes, using OLETF rat model was shown. Second, the influence of sucrose and ethanol on insulin secretion and insulin sensitivity was studied. Third, the relation between fat and diabetes was discussed. Especially the importance of difference in the quality of fat was emphasized. Fourth, the significance of the idea of glycemic index for preventing the absorption of carbohydrate was explained. Fifth, the application of dietary fiber for preventing diabetes was shown, using WBN/Kob rat model.

Animals↗
PubMed1995

[The effects of insulin and glucose on the utilization of non-esterified fatty acid in the resting rat skeletal muscle].

The present study was undertaken to clarify the effects of insulin and glucose on the utilization of non-esterified fatty acid (NEFA) in the resting rat skeletal muscle using the perfusion technique. The 24hr-starved and non-starved rat hind limbs were perfused for one hour with the perfusion mediums containing 1mM palmitate and various concentrations of glucose and insulin, and sampling was performed to calculate the clearance of NEFA (F value). In the absence of glucose, the F value of the starved rat hind limb was less than that of the non-starved rats, independently of insulin concentrations (0 and 125 microU/ml) in the perfusion medium (p < 0.02). Moreover, there was no influence of insulin on the F value in both the starved and the non-starved groups. In the presence of 13.9mM glucose, there were no statistically significant differences in the F value without insulin between the non-starved and starved groups. However, the F value was increased in the presence of 62.5 or 125 microU/ml insulin, compared with that in the absence of insulin (p < 0.001), although when the insulin concentration was elevated to 500 microU/ml, it was decreased. Both in the non-starved and the starved groups independently of insulin concentrations, the F value in the glucose-added condition was increased, compared with that in the absence of glucose. These results indicated that the utilization of NEFA in the resting rat skeletal muscle was facilitated by the moderate supply of glucose, although it was suppressed by the presence of abundant glucose.

Animals↗
PubMed1994

Can plasma glucose and nonesterified fatty acid be regulators of glucose utilization in skeletal muscle?

The effect of plasma glucose and nonesterified fatty acid (NEFA) on basal and insulin-stimulated glucose utilization in skeletal muscle was assessed by perfused hindlimb preparations. Two-month-old male Wistar rats were divided into four groups: starved, glucose-loaded, hypoglycemic and control. Diabetic rats were made by means of streptozotocin, and divided into three groups: non-treated, insulin-treated normoglycemic and insulin-treated hyperglycemic. The effect of NEFA on glucose clearance was also investigated by adding palmitate to the perfusate. Basal glucose utilization decreased with a rise in plasma glucose concentrations, and increased with a fall in them in each group. The available data strongly support the view that plasma glucose levels play an important role in the control of basal glucose utilization by the hindlimb muscle. In contrast, continuous hyperglycemia in the diabetic state decreased insulin-stimulated glucose utilization by the skeletal muscle, whereas an acute rise in plasma glucose concentrations in the glucose-load state did not. Palmitate stimulated basal glucose utilization, while it decreased insulin-stimulated glucose uptake. It was also clarified that it increased the affinity for glucose in the skeletal muscle in the basal state. This finding seems to indicate that NEFA has some influence on an increase in basal glucose utilization in starvation.

Animals↗
PubMed1993

Type 1 (insulin-dependent) diabetic patient with remarkable infiltration of lymphocytes to the islets.

We report the case of a 62-year-old woman who was admitted to our hospital with diabetic ketoacidosis. Her urinary C-peptide was 3.5 micrograms/day, HLA typing was DR9, and serum was positive for islet cell antibodies. There was no significant increase in the major viral titer. Pancreatic head tumor was suspected, and pancreaticoduodenectomy was performed. The pathology of this tumor was polycystic adenoma. We examined the surgical specimen from around the tumor histologically. The pancreatic islets had decreased in number. The immunohistochemical staining of islets for insulin, glucagon and somatostatin showed that the number of B cells had decreased remarkably, while A and D cells were preserved. Marked lymphocytic infiltration was observed in the islets. The majority of lymphocytes were helper/inducer and suppressor/cytotoxic T cells, which did not express HLA-DR antigen or interleukin-2 receptor. No NK cells were present in the islets. The present case, which was examined histologically in detail, is consistent with the previously proposed hypothesis that autoimmunity might play an important role in the pathogenesis of insulin-dependent diabetes mellitus.

Adenoma↗
PubMed1984

[The effect of methyleneblue on insulin and glucagon release stimulated by glucose and arginine in the isolated perfused rat pancreas].

To examine the role of NADPH in the release of insulin and glucagon, isolated rat pancreata were perfused with methyleneblue, which is known to oxidize NADPH. Hormonal release was stimulated by changes in arginine or glucose concentrations as follows. After establishing the basal secretion state during perfusion at various glucose levels for 10 min., pancreata were stimulated by the addition of arginine or a change in glucose concentration of the perfusate for 15 min. Conditions for the stimulation were: (A) addition of 10 mM arginine at constant 4 mM glucose concentration; (B) increase in glucose concentration from 2.8 mM to 11.1 mM, or (C) decrease in glucose concentration from 11.1 mM to 2.8 mM. In some experiments, methyleneblue was added throughout the perfusion period at 1 or 3 micrograms/ml. The effluent from the portal vein was collected over 1 minute intervals: Insulin and glucagon concentrations in the effluent were determined by radioimmunoassay. Insulin release. Stimulation by the addition of arginine and increased glucose concentration produced a typical biphasic insulin response. In both cases, 1 microgram/ml methyleneblue reduced the second phase, and 3 micrograms/ml methyleneblue inhibited both phases almost completely. Glucagon release: Stimulation by arginine and inhibition by increasing glucose concentration were not influenced by methyleneblue; however, glucagon release induced by lowering of glucose concentration was suppressed by 3 micrograms/ml of methyleneblue. Thus, methyleneblue specifically inhibits glucose- and arginine-induced insulin release while it has no effect on arginine-induced glucagon release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Amelioration of streptozotocin-induced diabetes in the rat by exercise-training: role of muscle glycogenolytic and glycolytic enzyme activity.

Streptozotocin-induced insulin deficient rats allowed to run at will had significantly (P less than 0.001) lower mean (+/- SEM) plasma glucose levels (12.1 +/- 0.9 vs 22.6 +/- 1.7 mM/l) than did equally insulin deficient sedentary rats. Muscle glycogen phosphorylase and synthase activities were similar in exercise-trained and sedentary diabetic rats, and were unchanged from control values. In contrast, muscle phosphofructokinase activity was reduced (P less than 0.001) in sedentary rats with insulin deficiency, and the defect was significantly reversed (P less than 0.01) when such rats were allowed to run spontaneously. These results are consistent with the view that the ability of exercise-training to attenuate the magnitude of hyperglycemia in streptozotocin-induced insulin deficiency is associated with an effect on a key regulatory enzyme in the glycolytic pathway.

Animals↗
PubMed1984

Insulin resistance in older rats.

Insulin-stimulated glucose utilization was estimated in vivo in 1.5-, 4-, and 12-mo-old rats with an insulin suppression test wherein the height of the steady-state plasma glucose ( SSPG ) concentration, at similar steady-state plasma insulin levels, provides a direct reflection of the efficiency of insulin-stimulated glucose disposal. In parallel studies, the effect of age on in vitro insulin-stimulated glucose uptake was assessed in perfused hindlimb preparations. In addition, changes in the activity of enzymes that regulate muscle glycolysis, glycogenesis, and glycogenolysis were determined in isolated soleus muscle. The results indicated that rats got heavier as they became older, and changes in weight were associated with parallel increases in mean (+/- SE) SSPG concentrations as rats grew from 1.5 (56 +/- 3 mg/dl) to 4 (172 +/- 6 mg/dl) to 12 mo of age (194 +/- 8 mg/dl). The age-related decline in in vivo insulin action was associated with a reduction in insulin action on muscle, and maximal insulin-stimulated glucose uptake by perfused hindlimbs of 12-mo-old rats was approximately 50% of the value seen with perfused hindlimbs from 1.5-mo-old rats. Soleus muscle enzyme activity also varied with age, with significant increases in glycogen synthase and decreases in glycogen phosphorylase documented. Furthermore, muscle glycogen phosphorylase activity, which fell during an insulin infusion in 1.5-mo-old rats, did not change when 12-mo-old rats were infused at comparable insulin levels. Finally, glycogen content was significantly increased (P less than 0.01) in soleus muscle from 12-mo-old rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1983

[Hyperglycemia and inhibition of glucose-induced insulin release in 6-aminonicotinamide treated rats].

The effects of 6-aminonicotinamide (6-AN) on blood glucose and insulin release were studied in rats. 6-AN at 4mg/100g body weight slowly raised blood glucose concentrations to a significantly higher level than the control values 6 hours after an intraperitoneal injection. At this time severe glucose intolerance and low IRI response were noticed during an intravenous glucose tolerance test. Adrenalectomized rats replaced by hydrocortisone also presented hyperglycemia, glucose intolerance and low IRI response during IVGTT under treatment with 6-AN but to a lesser extent than in the intact rats. In in vitro experiments, decreased insulin release from the perfused pancreata of rats pretreated with 6-AN was found both in the 1st and 2nd phases of response to glucose stimulation. These data indicate that 6-AN-induced hyperglycemia is attributed to the inhibition of insulin release in adrenalectomized rats except for the hypothetical effect of 6-AN which diminishes an action of insulin on cellular glucose transport.

6-Aminonicotinamide↗
PubMed1982

The effect of hypoxia on insulin and glucagon secretion in the perfused pancreas of the rat.

It has been reported that insulin secretion decreases during hypoxia both in vitro and in vitro, while an increase in glucagon secretion is found only in vivo. The effect of acute hypoxia on the secretion of glucagon and insulin was studied in the perfused rat pancreas. Phentolamine, an alpha-adrenergic blocker, was perfused during the period of hypoxia to elucidate the role of alpha-adrenergic stimulation. Sodium ATP and dibutyryl cAMP were also administered to study their effects on insulin and glucagon responses during hypoxia. In the present experiments, insulin secretion was suppressed while glucagon secretion was increased during hypoxia. Phentolamine did not cause any change in insulin of glucagon secretion. When dibutyryl cAMP was added, the increased glucagon secretion was reduced to the basal level, whereas the decreases in insulin secretion were not altered. The addition of sodium ATP reversed the hypoxia-induced decrease in insulin and the increase in glucagon secretion. These results suggest that a decrease in ATP production, which leads to impaired cAMP generation, pays a role in, and that alpha-adrenergic stimulation does not participate in the changes in, insulin and glucagon secretion during hypoxia in vitro.

Adenosine Triphosphate↗
PubMed1981

Adrenergic modulation of insulin and glucagon secretion from the isolated perfused rat pancreas.

In order to observe the effect of the adrenergic system on pancreatic glucagon secretion in the isolated perfused rat pancreas, phenylephrine, an alpha-adrenergic agonist, and isoproterenol, a beta-adrenergic agonist, were added to the perfused solution. 1.2 microM phenylephrine suppressed glucagon secretion at 2.8 mM glucose, and it also decreased insulin secretion at 11.1 mM glucose. 240 nM isoproterenol enhanced glucagon secretion not only at 2.8 mM glucose, but also at 11.1 mM glucose, as well as insulin secretion at 11.1 mM. In order to study the role of intra-islet noradrenalin, phentolamine, an alpha-adrenergic antagonist, and propranolol, a beta-adrenergic antagonist, were infused with the perfused solution. 10 and 100 microM phentolamine caused an increase in insulin secretion, and 25 microM propranolol decreased insulin secretion, while they did not cause any change in glucagon secretion. From these results, it can be concluded that alpha-stimulation suppresses not only insulin but also glucagon secretion, while beta-stimulation stimulates glucagon secretion, as well as insulin secretion. Intra-islet catecholamine may have some effect on the B cell, whereas it seems to have no influence on the A cell.

Animals↗