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Biomedical subjects

W Y Fujimoto

Publications and source records attributed to W Y Fujimoto.

At least 73 records · Page 4Linked to original sources
PubMed1990

Cigarette smoking, adiposity, non-insulin-dependent diabetes, and coronary heart disease in Japanese-American men.

PURPOSE: Coronary heart disease has been described to be increased with both glucose intolerance and cigarette smoking. All three of these have also been reported to be associated with central adiposity (disproportionate deposition of fat on the trunk compared to the extremities). The purpose of this analysis was to determine the relationship of cigarette smoking to glucose intolerance and coronary heart disease, the relationship of cigarette smoking to risk factors such as adiposity, body fat distribution, and plasma lipoprotein and insulin levels, the relationship of cigarette smoking to these risk factors independent of disease status, and whether these risk factors could account for any of the relationship between cigarette smoking and disease status. PATIENTS AND METHODS: The study design was cross-sectional. The study sample contained 219 middle-aged and elderly Japanese-American men: 77 with normal and 74 with impaired glucose tolerance and 68 with type II diabetes. There were 54 men with coronary heart disease. A detailed smoking history was obtained. Glucose tolerance status was established by medical history and a 75-g oral glucose tolerance test. Coronary heart disease was determined by medical history and a resting electrocardiogram. Adiposity and fat distribution measurements were body mass index (kg/m2), skinfold thicknesses, body circumferences, and cross-sectional fat areas by computed tomography. Levels of insulin, C-peptide, cholesterol (total, low-density lipoprotein [LDL], high-density lipoprotein [HDL], HDL2, HDL3, very-low-density lipoprotein [VLDL]), and triglyceride (total, VLDL) were measured in fasting blood specimens. RESULTS: A central pattern of body fat was associated with both non-insulin-dependent diabetes mellitus and coronary heart disease. Smoking history was related to both adiposity and body fat distribution, and was strongly related to coronary heart disease but not to diabetes. Past smokers who had smoked up to a month ago were the heaviest while present smokers who were currently smoking or had smoked within the past month were the leanest. However, although present smokers had reduced amounts of fat, this was attributable to those present smokers without heart disease. Present smokers with heart disease were not as lean and had increased amounts of intra-abdominal fat. Past smokers had the greatest amount of central fat and this was attributable to those with heart disease. By two-way (smoking history and coronary heart disease status) analysis of covariance, smoking history was significantly related only to subcutaneous fat disposition on the chest and abdomen independent of coronary heart disease, while coronary heart disease status was strongly related to plasma levels of insulin C-peptide, VLDL, HDL, HDL2, and HDL3 cholesterol, and total and VLDL triglyceride, independent of smoking history. Further analysis showed that none of the body fat variables could account for the risk of coronary heart disease associated with smoking history. Higher fasting plasma C-peptide levels in past smokers accounted statistically for part of the risk of coronary heart disease associated with cigarette smoking. However, this effect was not mediated by any of the body fat measurements. CONCLUSIONS: Disproportionately increased intra-abdominal fat is related to coronary heart disease but not to smoking history. Smoking history is related to coronary heart disease but not to diabetes. Weight gain is associated with smoking cessation and appears to be concentrated in the central subcutaneous regions, especially for those who have coronary heart disease. Weight gain associated with cessation of smoking appears to be unrelated to atherogenic changes in lipids, lipoproteins, or insulin. Other pathogenic processes must be considered in the association between smoking and coronary heart disease.

Adipose Tissue↗
PubMed1990

Diet of second-generation Japanese-American men with and without non-insulin-dependent diabetes.

Second-generation Japanese-American (Nisei) men have rates of non-insulin-dependent diabetes mellitus four times higher than men in Japan, suggesting a role for environmental factors in the etiology of this disease. Dietary intake was assessed for 229 Nisei men with diabetes (DM, n = 78), impaired glucose tolerance (IGT, n = 72), and normal glucose tolerance (NGT, n = 79). The diet of Nisei men with DM compared with men with IGT or NGT was similar in kilocalories but higher in fat and protein. Absence of diabetes was self-reported by 153 men (N-entry) of which 76 were confirmed to have NGT and 17 were discovered to have DM. Animal-protein and -fat intakes were significantly higher in N-entry DM men than in N-entry NGT men. Overall the Nisei diet, particularly that of Nisei men with DM, resembled more the diet of US men than men in Japan.

Aging↗
PubMed1990

Association of fasting glucose levels with a delayed secretion of insulin after oral glucose in subjects with glucose intolerance.

Two hundred and nineteen second generation Japanese-American men were classified with a 75-g oral glucose tolerance test: 77 with normal glucose tolerance, 74 with impaired glucose tolerance (IGT), and 68 with noninsulin-dependent diabetes mellitus (NIDDM). The peak insulin response to the oral glucose load was progressively delayed with each of the 3 glucose tolerance categories. A similar finding was observed with the peak C-peptide response to oral glucose, except for the absence of distinction between IGT and NIDDM. Variables measuring the initial rate of insulin or C-peptide secretion (0-30 min) after oral glucose also demonstrated a progressive diminution with increasing glucose intolerance. The relative incremental insulin response at 30 min and the relative incremental C-peptide response at 30 min were highly correlated with the fasting glucose levels (r = -0.61 and r = -0.62; P less than 0.0001, respectively). Variables measuring the 0-30 min secretory response had high variances, whereas the variance for fasting glucose was low. Twelve men who were initially classified as IGT subsequently developed NIDDM. These 12 men had significantly higher fasting glucose levels at baseline than the remaining men who did not develop diabetes, but the 30 min secretory parameters after oral glucose, although lower in those who subsequently developed diabetes, were not significantly different at baseline. However, if fasting glucose is used as a surrogate measure of secretory response, these 12 men appear to have had an impairment of oral glucose-stimulated insulin secretion antedating the development of NIDDM. The inability of the secretory parameters to detect the abnormality may be due to a type II statistical error, which may be resolved by a larger sample size.

Asian↗
PubMed1990

Evidence of cosecretion of islet amyloid polypeptide and insulin by beta-cells.

Islet amyloid polypeptide (IAPP) has been identified as the major constituent of the pancreatic amyloid of non-insulin-dependent diabetes mellitus (NIDDM) and is also present in normal beta-cell secretory granules. To determine whether IAPP is a pancreatic secretory product, we measured the quantity of IAPP-like immunoreactivity (IAPP-LI), insulin, and glucagon released into 5 ml of incubation medium during a 2-h incubation of monolayer cultures (n = 5) of neonatal (3- to 5-day-old) Sprague-Dawley rat pancreases under three conditions: 1.67 mM glucose, 16.7 mM glucose, and 16.7 mM glucose plus 10 mM arginine and 0.1 mM isobutylmethylxanthine (IBMX). The quantity of IAPP-LI, insulin, and glucagon in the cell extract was also determined. Mean +/- SE IAPP-LI in the incubation medium increased from 0.041 +/- 0.003 pmol in 1.67 mM glucose to 0.168 +/- 0.029 pmol in 16.7 mM glucose (P less than 0.05) and 1.02 +/- 0.06 pmol in 16.7 mM glucose plus arginine and IBMX (P less than 0.05 vs. 1.67 or 16.7 mM glucose). Insulin secretion increased similarly from 4.34 +/- 0.27 to 20.2 +/- 0.6 pmol (P less than 0.05) and then to 135 +/- 5 pmol (P less than 0.05 vs. 1.67 or 16.7 mM glucose). Glucagon release tended to decrease with the increase in glucose concentration (0.39 +/- 0.01 vs. 0.33 +/- 0.02 pmol, P less than 0.1), whereas with the addition of arginine and IBMX to high glucose, glucagon release increased to 1.32 +/- 0.03 pmol (P less than 0.05 vs. 1.67 or 16.7 mM glucose).(ABSTRACT TRUNCATED AT 250 WORDS)

Amyloid↗
PubMed1990

Association of elevated fasting C-peptide level and increased intra-abdominal fat distribution with development of NIDDM in Japanese-American men.

The Japanese-American population of King County, Washington, is known to have a high prevalence of non-insulin-dependent diabetes mellitus (NIDDM). As part of a community-based study, we reexamined 146 second-generation Japanese-American men who had been initially classified as nondiabetic. At a mean follow-up period of 30 mo, 15 men had developed NIDDM, and 131 remained nondiabetic. The variables measured at the initial visit that distinguished the 15 diabetic men from the 131 nondiabetic men were older age, higher serum glucose level at 2 h after 75 g oral glucose, higher fasting plasma C-peptide level, and increased cross-sectional intra-abdominal fat area as determined by computed tomography. Both older age and higher 2-h glucose levels are variables that have been associated with the development of NIDDM, but the association of higher fasting C-peptide level and greater intra-abdominal fat area with subsequent development of NIDDM were new observations. The elevated fasting C-peptide level persisted after adjustment for fasting serum glucose. The elevated C-peptide level represents hypersecretion of insulin and was interpreted to reflect a compensatory response to an underlying insulin-resistant state that antedates the development of NIDDM. The fasting C-peptide level was correlated with the intra-abdominal fat area, suggesting that the intra-abdominal fat area may be associated with insulin resistance. Thus, in individuals who develop NIDDM, insulin resistance, increased insulin secretion, and increased intra-abdominal fat are present before diabetic glucose tolerance can be demonstrated.

Abdomen↗
PubMed1989

Plasma insulin levels in Japanese and Japanese-American men with type 2 diabetes may be related to the occurrence of cardiovascular disease.

Sixty-eight second-generation Japanese-American (Nisei) men 45-74 years old and 26 Tokyo Japanese men 40-72 years old with type 2 diabetes were given 75 g glucose by mouth, and their venous blood levels of glucose and insulin were measured at 0, 30, 60, 90, 120, and 180 min. Blood glucose levels were similar for the two groups but the Nisei had higher levels of insulin at all time points (P less than 0.006). The Nisei men had a higher mean body mass index (P less than 0.001) and the Tokyo men had had diabetes for a longer duration (P less than 0.001). Data were also compared following selection of a subgroup of Nisei men (n = 39) with a diabetes duration of 2-25 years, making this group more similar to the Tokyo men with respect to this variable. The Nisei still had significantly higher plasma insulin levels. Because of a significant (P less than 0.01) positive correlation between plasma insulin and body mass index in Nisei, but not in Tokyo men, data comparing the Nisei subgroup and Tokyo men were re-examined by analysis of covariance. With an adjustment for body mass index in the analysis, all differences in plasma insulin, except for the fasting insulin level, were no longer significant between the Nisei and Tokyo men, suggesting that body mass index was responsible for these differences.

Aged↗
PubMed1989

Early-life background and the development of non-insulin-dependent diabetes mellitus.

The relationship of early-life background factors to type 2, or non-insulin-dependent, diabetes mellitus (NIDDM) was examined with reference to family history of diabetes in two groups of Nisei (U.S. born/raised Japanese American) men from King County, Washington with identical mean (+/- S.E.M.) ages: 78 with NIDDM, 61.6 (+/- 0.7) years of age; and 79 with normal glucose tolerance (NGT), 61.6 (+/- 0.6) years of age. The early-life variables were birthplace, parents' education, father's occupation and mother's employment status during subject's childhood, sibship size, son birth order, physical activity and weight assessed for ages 15-20 years, and educational achievement. Multivariate logistic regression models were used to test for the effect of each variable on the risk for diabetes in the presence of other variables. Results are presented as odds ratios (OR) with 95% confidence intervals (CI). Significantly higher risk for NIDDM was found with urban birthplace (vs. rural, OR = 2.09, 95% CI = 1.37-3.19), parents' education above primary level (vs. primary level or less, OR = 1.64, 95% CI = 1.08-2.50), mother being employed (vs. housewife, OR = 2.17, 95% CI = 1.43-3.45), subject being less active-lean as a youth (vs. more active-lean, OR = 1.69, 95% CI = 1.11-2.63), and subject's not attaining a college degree (vs. college degree, OR = 2.17, 95% CI = 1.41-3.33). In separate analyses of the early-life variables by family history of diabetes, the interplay of environmental influences with familial predisposition to NIDDM is evident. The developmental background of NIDDM is discussed with reference to the concept of phenotype amplification within the context of the effects of westernization.

Aged↗
PubMed1989

Fatness, fat distribution, and glucose tolerance in second-generation Japanese-American (Nisei) men.

The association between amount and distribution of fat and glucose tolerance was examined in 229 second-generation Japanese-American men. According to the results of a 75-g oral glucose tolerance test and by World Health Organization (WHO) diagnostic criteria, 79 men were normal, 72 had impaired glucose tolerance (IGT), and 78 had noninsulin-dependent diabetes mellitus. Diagnostic groups were compared by using 10 measures of fatness derived from body mass indices, skinfold thicknesses, and fat areas, which were determined by computed tomography. IGT men were fatter than normal men on five measures; diabetic men were fatter on four and group differences were marginally significant (p greater than or equal to 0.03). Diabetic subjects had the largest deposits of subscapular (p = 0.01) and more biceps fat than normal men (p = 0.01); IGT men had more midthigh fat than diabetic men (p = 0.01). The diabetes and IGT groups possessed more intraabdominal fat (p = 0.003). For serum glucose levels there was an interaction between body mass index and subscapular fat.

Adipose Tissue↗
PubMed1989

Defective enzyme protein in lipoprotein lipase deficiency.

A monoclonal antibody to lipoprotein lipase (LPL) has been used in an enzyme-linked immunosorbent assay (ELISA) for LPL protein mass. Measurement of LPL immunoreactive mass in pre- and postheparin plasma distinguished three classes of abnormalities in patients with classical deficiency of lipoprotein lipase activity. The class I defect consisted of the absence of LPL immunoreactive homodimer in pre- and postheparin plasma compatible with a potential 'null allele'. Patients with a class II defect had almost no LPL immunoreactive mass in preheparin plasma but showed an increase in their LPL mass of 68 +/- 23 ng ml-1 (mean +/- SD) after heparin. Patients with the class III defect had considerable amounts of LPL immunoreactive material in preheparin plasma (159 +/- 190 ng ml-1). Heparin administration, however, caused very little additional release of LPL into the plasma (16 +/- 51 ng ml-1). Thus although both class II and class III patients had an LPL protein with abnormal catalytic activity, class III patients also appeared to have a defect in heparin binding of LPL. To test this hypothesis, postheparin plasma of classes II and III patients was analysed by heparin-Sepharose chromatography. In contrast to class II patients, the LPL immunoreactive mass of class III patients did not show affinity for the heparin and eluted in the column void volume, suggesting the class III defect is also associated with a defect in heparin binding.

Binding Sites↗
PubMed1989

Oscillatory insulin secretion in perifused isolated rat islets.

After a step-function increase in glucose concentration, insulin secretion by perifused isolated rat islets of Langerhans showed oscillations superimposed on the well-known first- and second-phase secretory components. The oscillations were sustained for the length of the experiment and corresponded to at least four cycles. This established the existence of an oscillatory pacemaker with a narrow dispersion of periodicities intrinsic to the islets and showed that synchronization of islet action could be achieved by a step-function increase in glucose concentration. The observed period of 16 min is similar to the period of oscillatory insulin secretion in a number of intact organisms. This argues for identity of pacemakers in vivo and in isolated islets. This means that neural or other forms of interislet communication are not prerequisites for oscillatory insulin secretion. Theophylline increased the length of the oscillatory period, suggesting the periodicity of the pacemaker of insulin secretion can be metabolically regulated. This observation also provided a basis for explaining fine tuning of oscillatory periods by the nervous system.

Animals↗
PubMed1989

Effects of glucagonlike peptide I-(7-36) on release of insulin, glucagon, and somatostatin by rat pancreatic islet cell monolayer cultures.

Glucagonlike peptide I (GLP-I-(7-36] is cleaved from proglucagon in ileal epithelial cells and increases in human plasma after nutrient ingestion. This peptide has been shown to stimulate insulin secretion in vitro and in vivo and thus potentially acts as an incretin. To characterize its action on islet cells, the release of insulin, glucagon, and somatostatin by rat pancreatic islet monolayer cultures at varying concentrations of GLP-I-(7-36) was measured. The interaction of GLP-I-(7-36) with nutrient substrates was assessed by adding amino acids and differing glucose concentrations to the cultures. Islet cell cultures (n = 5) were incubated for 1 h in medium containing 1.67 or 16.7 mM glucose or 1.67 mM glucose supplemented with amino acids and GLP-I-(7-36) at 10(-13)-10(-7) M. Hormone release was compared with control cultures containing no GLP-I-(7-36); 1.67-16.7 mM glucose with and without GLP-I-(7-36) at 10(-11) M; and 1.67, 3.3, 8.3, or 11.1 mM glucose alone or supplemented with amino acids, GLP-I-(7-36) 10(-11) M, or both amino acids and GLP-I-(7-36). In medium with 1.67 or 16.7 mM glucose or 1.67 mM glucose and amino acids, GLP-I-(7-36) increased insulin secretion two- to threefold over control at concentrations of 10(-9), 10(-11), and 10(-12) M, respectively. In medium with increasing concentrations of glucose, GLP-I-(7-36) at 10(-11) M significantly increased insulin secretion at glucose concentrations greater than or equal to 3.34 mM.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Phasic effects of glucose, p-hydroxymercuribenzoate, and lysophosphatidylcholine on insulin secretion from HIT cells.

Monolayer cultures of HIT cells were superfused to examine phasic insulin secretion. A biphasic pattern of insulin secretion was observed when cells were stimulated with a constant glucose concentration as low as 0.28 mM, with increasing stimulation at 0.56, 1.7, and 5.6 mM glucose. Higher glucose concentrations did not increase insulin secretion. In the absence of glucose, p-hydroxymercuribenzoate (15, 30, and 50 microM), which blocks the reacylation of lysophospholipids with arachidonic acid, also evoked a concentration-dependent biphasic release of insulin. Lysophosphatidylcholine (50, 75, and 100 micrograms/ml) also caused a concentration-dependent biphasic release of insulin in the absence of glucose. These observations were similar to those previously reported for superfused monolayer culture of rat islet cells and suggest that the HIT cell is a beta-cell line that may be valuable in the further examination of the relationships among glucose, phospholipid metabolism, and insulin secretion. The data are consistent with the hypothesis that glucose-stimulated release of lysophospholipids may be important in initiation of the biphasic pattern of glucose-stimulated insulin release.

Animals↗
PubMed1989

Elevated plasma glucose and lowered triglyceride levels from omega-3 fatty acid supplementation in type II diabetes.

We studied the effect of omega-3 fatty acids (omega 3FA) on glucose homeostasis and lipoprotein levels in eight type II (non-insulin-dependent)-diabetic subjects ingesting 8 g/day omega 3FA for 8 wk as marine-lipid concentrate capsules. After omega 3FA supplementation, fasting plasma glucose levels increased 22% (P = .005) and meal-stimulated glucose increased 35% (P = .036). The percentage of glucose elevation correlated with percentage ideal body weight (r = .73, P = .04). No significant changes were seen in fasting or meal-stimulated plasma insulin, glucose disposal, or insulin-to-glucagon ratios. Very-low-density lipoprotein cholesterol and triglyceride (TG) levels showed consistent reductions of 56% (P less than .001) and 42% (P less than .001), respectively, after omega 3FA supplementation. Total cholesterol levels decreased 7% (P less than .05) without alteration in low- or high-density lipoprotein cholesterol. Thus, omega 3FA supplementation at a dose of 8 g/day significantly improves plasma TG levels but increases fasting and meal-stimulated glucose concentrations in the type II diabetic patient not treated with insulin or sulfonylurea agents. Marine-lipid concentrate capsules supplying large amounts of omega 3FAs should be used cautiously in the type II diabetic patient.

Aged↗
PubMed1989

Type 2 diabetes, impaired glucose tolerance, and hypertension in offspring of migrants and the structure of the population of origin.

Data collected from Nisei men and women, offspring of immigrants to the United States from Japan, were examined for evidence of possible genetic heterogeneity in Japan with respect to type 2 diabetes or non-insulin-dependent diabetes mellitus (NIDDM), impaired glucose tolerance (IGT), and hypertension. The subjects were 391 men and women with a mean age of 62.0 (+/- 0.3) years. Patterns of disease expression in the Nisei with respect to the origins in Japan of their parents indicated that the genetic basis for NIDDM may be more frequent in northern Honshu than in southwestern Honshu, whereas that for IGT may be more frequent in southwestern Honshu. Further analyses indicate that the pattern for IGT is restricted to men. Hypertension appears more frequently in persons with parents from northern Honshu and less frequently in women but not in men from southwestern Honshu. For men an analysis of age and family history of diabetes by oral glucose diagnostic category revealed the presence of a group of younger men with IGT but, surprisingly, no family history of diabetes. Thus the data show an apparent lack of the consistency expected if diabetes and IGT simply represent stages of one disease entity. We suggest that IGT may represent a heterogeneous category including both an early or transitional stage of NIDDM and another condition found primarily in men in which less severe glucose tolerance appears and with which hypertension may be associated. Data on ancient settlement in Japan suggest a possible historical basis for the patterns found.

Blood Glucose↗
PubMed1988

Electrodiagnosis of diabetic peripheral polyneuropathy. A multivariate analytic approach.

Traditional univariate comparisons of nerve conduction data against standard norms may produce conflicting estimates of the presence or absence of a diabetic neuropathy, depending upon the data obtained and the specific nerves sampled. Alternatively, a multivariate analytic approach, using discriminant functions, provides a useful single measure of the degree of neuropathy determined as a weighted combination of the available data. The weights are derived from the linear discriminant function, which maximizes statistical separation of diabetic and nondiabetic subject groups. In this study, 12 electrophysiologic attributes are used to generate a single discriminant function that clearly separates diabetic from nondiabetic subjects and is interpretable as a neuropathic index. Each individual's index of diabetic neuropathy (I) can be quantified as follows: (Formula: see text) where Ai is the original electrophysiologic attribute (i = 12), ai is the coefficient for each attribute that defines the discriminant function and C is a constant specific for that function. For the first time, the degree of diabetic neuropathy can thus be quantified for purposes of comparison and correlation with other quantifiable clinical/somatic measures of diabetes. The index allows for a higher percentage of type II diabetic patients to be classified as neuropathic than previously described and enables determination of degree of neuropathy is affected individuals by an interpolative method.

Analysis of Variance↗
PubMed1988

Friedewald's LDL-cholesterol estimation formula in a Japanese American population.

Friedewald's formula is often used to estimate low density lipoprotein cholesterol (LDL-c) when direct measurement is not available. In this equation, the ratio of triglyceride (TG): cholesterol (C) in very low density lipoprotein (VLDL) is assumed to be 5:1. Recently it has been reported that in native Japanese the formula provided a better fit if this ratio is taken to be 4:1. The application of the formula was therefore examined in a sample of 229 second-generation Japanese American (Nisei) men. In this population, the 5:1 ratio of TG:C in VLDL was found to be appropriate. Thus the findings reported for native Japanese do not appear to be generally applicable to all Japanese populations.

Aged↗
PubMed1987

24-h catecholamine excretion: relationships with age and weight.

24-hour urines were obtained from groups of volunteer subjects recruited from populations in the UK, USA, Nigeria and the South Pacific. Urines were collected during the course of normal daily activities. HPLC/electrochemical detection was used to measure concentrations of adrenaline and noradrenaline in each urine. Calculated 24-h output of catecholamines was tested for significant linear regression relationships with age, weight and 24-h urine volume in each population. Noradrenaline excretion tended to be positively related to age and to body wt. Adrenaline excretion tended to show little or no relationship with either age or body wt. Relationships based on catecholamine excretion/U creatinine were notably different to those based on absolute catecholamine excretion. Differences were observed in the nature and strength of the relationships in the different populations, indicating the likely importance of interactions with other factors.

Adult↗