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T Sane

Publications and source records attributed to T Sane.

At least 37 records · Page 2Linked to original sources
PubMed1996

Postmarathon paradox: insulin resistance in the face of glycogen depletion.

Acute physical exercise enhances insulin sensitivity in healthy subjects. We examined the effect of a 42-km marathon run on insulin sensitivity and lipid oxidation in 19 male runners. In the morning after the marathon run, basal serum free fatty acid concentration was 2.2-fold higher, muscle glycogen content 37% lower (P < 0.01), glycogen synthase fractional activity 56% greater (P < 0.01), and glucose oxidation reduced by 43% (P < 0.01), whereas lipid oxidation was increased by 55% (P < 0.02) compared with the control study. During euglycemic-hyperinsulinemic clamp, whole body glucose disposal was decreased by 12% (P < 0.01) because of a 36% lower glucose oxidation rate (P < 0.05), whereas the rate of lipid oxidation was 10-fold greater (P < 0.02) than in the control study. After the marathon, muscle glycogen content correlated positively with lipid oxidation (r = 0.60, P < 0.05) and maximal aerobic power (Vo2peak; r = 0.61, P < 0.05). Vo2peak correlated positively with basal lipid oxidation (r = 0.57, P < 0.05). In conclusion, 1) after the marathon run, probably because of increased lipid oxidation, the insulin-stimulated glucose disposal is decreased despite muscle glycogen depletion and the activation of glycogen synthase; 2) the contribution of lipid oxidation in energy expenditure is increased in proportion to physical fitness; 3) these adaptations of fuel homeostasis may contribute to the maintenance of physical performance after prolonged exercise.

Adult↗
PubMed1995

LDL particle size in mildly hypertriglyceridemic subjects: no relation to insulin resistance or diabetes.

We examined 18 Type 2 diabetic and 19 non-diabetic subjects in order to determine the association between insulin resistance and LDL particle size distribution in mildly hypertriglyceridemic and hyperinsulinemic subjects with and without Type 2 diabetes. Insulin sensitivity of the patients was characterized by their insulin-stimulated glucose uptake rate determined by euglycemic clamp technique. LDL particle size distribution was determined by nondenaturing polyacrylamide gradient gel electrophoresis. Type 2 diabetic and non-diabetic subjects had closely similar serum lipid and lipoprotein concentrations as well as the mean particle diameters of the major LDL peak (246 +/- 6 A and 244 +/- 6 A, respectively). To evaluate the effect of insulin resistance on LDL particle size the participants were categorized into two subgroups using the median of their insulin-stimulated glucose uptake rate (14.67 mumol/kg/min) as a cut-off point. Neither lipid and lipoprotein concentrations nor the LDL particle size distributions differed between the more insulin resistant group (nine diabetic and nine non-diabetic subjects) and less insulin resistant group (nine diabetic and ten non-diabetic subjects). LDL particle size was not associated with the insulin-stimulated glucose uptake rate or with the mean 24-h concentration of serum insulin. Mean 24-h concentration of serum triglycerides was the strongest discriminator for LDL particle size (r = -0.44, P < 0.01). In conclusion, neither Type 2 diabetes nor insulin resistance seem to have any direct effect on LDL particle size in mildly hypertriglyceridemic subjects. The fact that LDL particle size was associated with serum triglycerides indicates that the effect of diabetes and insulin resistance on LDL particle size could be explained by the effects of insulin resistance and/or hyperinsulinism on VLDL metabolism.

Blood Glucose↗
PubMed1995

Decreasing triglyceride by gemfibrozil therapy does not affect the glucoregulatory or antilipolytic effect of insulin in nondiabetic subjects with mild hypertriglyceridemia.

We studied the effects of gemfibrozil on glucose and fatty acid metabolism in subjects with mild endogenous hypertriglyceridemia. Twenty subjects (serum triglycerides, 3.2 +/- 1.4 mmol/L; age, 52 +/- 7 years; body mass index, 27.8 +/- 1.8 kg/m2) were randomly allocated to receive either placebo or gemfibrozil 1,200 mg daily for 12 weeks in a double-blind study. Gemfibrozil decreased serum total and very-low-density lipoprotein (VLDL) triglycerides by 53% and 57%, respectively, and serum apolipoprotein (apo) B concentration by 21%. Gemfibrozil had no effect on the diurnal concentration of free fatty acids (FFA). Neither did gemfibrozil change diurnal blood glucose or serum insulin concentrations. The endogenous glucose production rate remained unchanged in both groups during the treatment period, and was similarly suppressed by hyperinsulinemia. The rate of insulin-induced whole-body glucose disposal increased similarly both before (basal 10.8 +/- 1.8, low-dose insulin 10.5 +/- 2.1, and high-dose insulin 20.9 +/- 11.9 mumol.kg-1.min-1) and after (11.1 +/- 1.7, 10.7 +/- 1.2, and 18.6 +/- 7.9, respectively) gemfibrozil treatment. Rates of oxidative and nonoxidative glucose metabolism remained unchanged during gemfibrozil treatment. Basal pretreatment and posttreatment FFA turnover rates were similar in both study groups, as were the rates of substrate oxidation. In summary, gemfibrozil proved to be an effective serum triglyceride-lowering agent in patients with mild hypertriglyceridemia, but had no effect on the insulin sensitivity of glucose metabolism or of antilipolysis. These data support the idea that triglycerides per se do not cause insulin resistance, and that the triglyceride-lowering effect of gemfibrozil is not mediated via antilipolytic action.

Analysis of Variance↗
PubMed1995

Effect of gemfibrozil on the regulation of HDL subfractions in hypertriglyceridaemic patients.

OBJECTIVES: To study changes of HDL subfractions and their regulation during gemfibrozil treatment in hypertriglyceridaemia. DESIGN: Twenty patients with hypertriglyceridaemia were randomized to receive either 1200 mg day-1 gemfibrozil or placebo for 3 months. After a 6-week, single-blind placebo period, the patients were randomized to receive either gemfibrozil or placebo for 3 months in a double-blind study. SETTING: The patients were studied as outpatients in the Third Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland. MAIN OUTCOME MEASURES: Ultracentrifugally isolated HDL subclasses; concentrations of apoA-I, apoA-II, LpA-I and LpA-I:A-II particles; post-heparin plasma lipoprotein lipase (LPL), hepatic lipase (HL) and plasma cholesteryl ester transfer protein (CETP) activities; phospholipid transfer protein (PLTP) and lecithine cholesteryl acyltransferase (LCAT) activities were measured in plasma from six patients from both groups. RESULTS: Gemfibrozil increased the concentration of HDL cholesterol (+11.1%) because of the rise of HDL3 cholesterol (34.5%, P < 0.01). The concentration of LpA-I particles was reduced during gemfibrozil treatment (-12.4%, P < 0.05), while that of apoA-II increased (+12.3%, P < 0.01). The LpA-I to LpA-I:A-II ratio decreased significantly in the gemfibrozil group (-18.9%, P < 0.01). Gemfibrozil increased LPL and HL activities by 18.2% (P < 0.05) and by 19.6%, respectively. Plasma CETP activity was also increased during gemfibrozil treatment (+15.8%, P < 0.05). CONCLUSION: The gemfibrozil-induced elevation of HDL3 and apoA-II may reflect the combined action of LPL, HL and CETP on plasma HDL metabolism.

Adult↗
PubMed1994

No evidence for linkage between familial hypertriglyceridemia and apolipoprotein B, apolipoprotein C-III or lipoprotein lipase genes.

Familial hypertriglyceridemia has been suggested to be an autosomal dominant condition with age-dependent penetrance, but so far the underlying defective gene has not been elucidated. We examined the possible role of three candidate gene loci by linkage analysis in six Finnish families with familial clustering of hypertriglyceridemia. The probands were initially recruited from a group of hyperlipidemic outpatients after measurement of serum triglyceride concentrations exceeding 2.00 mmol/l on two occasions. Altogether, 71 subjects were included in the linkage analyses. Bi- or multiallelic DNA polymorphisms were used as markers for the apolipoprotein B gene (chromosome 2), lipoprotein lipase gene (chromosome 8), and apolipoprotein A-I/C-III/A-IV gene cluster (chromosome 11). Linkage analysis was performed by applying two alternative phenotyping models, one adopting quantitative serum triglyceride concentrations and another using qualitative classification of the subjects into hypertriglyceridemic, normotriglyceridemic, and borderline hypertriglyceridemic groups. Using either approach, the cumulative lod scores of each of the three candidate genes in the six families were less than -2.0 at the recombination fraction 0.0. These results suggest that none of the candidate genes investigated is involved in familial clustering of hypertriglyceridemia in our study.

Adult↗
PubMed1994

Hyponatremia after transsphenoidal surgery for pituitary tumors.

We studied the incidence of postoperative hyponatremia in 91 consecutive patients (44 males and 47 females; age, 45 yr; range, 12-76) operated on transsphenoidally for pituitary tumors. A postoperative serum sodium concentration less than 135 mmol/L (the lowest, 109 mmol/L) was observed in 32 (35%) patients. Hyponatremia occurred most commonly in patients operated on for Cushing's disease (11 of 18 patients; 61%). Hyponatremia was symptomatic in 18 (56%) of the patients. Neither the size nor the operability of the tumor or transient postoperative polyuria predicted the development of hyponatremia. Hyponatremia was first observed on the sixth or seventh postoperative day. The patients were treated with water restriction and by increasing the hydrocortisone replacement dose in the case of ACTH deficiency, and recovery took place, on the average, within 5 days. High urinary osmolality and plasma arginine vasopressin concentration during hyponatremia in a subgroup of study patients with these measurements indicated that inappropriate vasopressin secretion was involved in the pathogenesis of hyponatremia. In conclusion, postoperative hyponatremia after transsphenoidal surgery is common and may put the patients at increased risk of severe hyponatremic symptoms. Therefore, all patients should be screened for serum electrolytes for 1 week after transsphenoidal surgery.

Adenoma↗
PubMed1993

Does familial hypertriglyceridemia predispose to NIDDM?

OBJECTIVE: To determine the 10-yr incidence of impaired glucose tolerance and NIDDM in families with a clustering of endogenous hypertriglyceridemia. RESEARCH DESIGN AND METHODS: The prospective population study, where the oral glucose tolerance test and the measurement of serum lipids and lipoproteins were performed at the baseline examination and after the 10-yr follow-up, was conducted on 56 subjects (17-60 yr of age at the baseline). The subjects were from six pedigrees with a clustering of endogenous hypertriglyceridemia, and 47 of these subjects attended the follow-up 10 yr later. RESULTS: In the study families, the prevalence of glucose intolerance and NIDDM increased from 15 to 49% (P < 0.001) and from 2 to 21% (P < 0.001), respectively, over the 10-yr period. When grouped according to the baseline serum triglyceride tertiles, 76% (P < 0.01) of the family members with highest serum triglycerides were glucose intolerant (29% impaired glucose tolerance, 47% NIDDM) at follow-up compared with 20% of those with lowest serum triglycerides. In discriminant analysis, including age, body mass index, treatment with thiazides and beta-blocking agents, and 2-h serum insulin concentration, the baseline serum triglycerides still remained as an independent predictor of development of impaired glucose tolerance and NIDDM. CONCLUSIONS: Families with a clustering of hypertriglyceridemia are at increased risk of NIDDM, and in these families elevation of serum triglycerides serves as a risk marker of glucose intolerance and NIDDM.

Adult↗
PubMed1992

One-year response to evening insulin therapy in non-insulin-dependent diabetes.

We studied the 1-year response and predictors of the response to combination therapy with evening insulin and oral agents in NIDDM patients with a secondary failure. Injection of intermediate-acting (Monotard HM) or long-acting (Ultratard HM) insulin was added to previous oral therapy in 17 diabetics (of mean age (+/- SD) 54 +/- 2 years, BMI 27.6 +/- 0.5 kg m-2). The initial insulin dose was in the range 10-16 U, and the mean dose was 23 +/- 2 U d-1 at 12 months. During the year, combination therapy reduced the mean fasting blood glucose concentration (12.7 +/- 0.6 vs. 8.4 +/- 0.7 mmol l-1, P less than 0.001) and HbA1 (10.7 +/- 0.3 vs. 9.8 +/- 0.4%, P less than 0.01). Body weight increased by 4.4 +/- 0.7 kg (P less than 0.001). The serum cholesterol concentration decreased by 14% (P less than 0.01), but serum triglyceride and HDL-cholesterol levels remained unchanged. Elevation of serum triglycerides and plasma free fatty acids (FFAs) at baseline predicted a poor long-term outcome to this mode of therapy. In conclusion, the addition of evening injections of insulin to oral therapy improves glycaemic control in poorly controlled NIDDM patients. However, initial hypertriglyceridaemia predicts a poor long-term outcome to evening insulin supplementation.

Adult↗
PubMed1992

Fuel and fluid homeostasis during long-term exercise in healthy subjects and type I diabetic patients.

OBJECTIVE: This study was designed to examine metabolic and hormonal effects of long-term exercise in healthy subjects and insulin-dependent (type I) diabetic patients. RESEARCH DESIGN AND METHODS: Two studies were performed. First, 16 healthy males (32 +/- 3 yr) were studied during a semitriathlon competition (2 km swimming, 90 km biking, and 21 km running). Second, 9 type I diabetic males (41 +/- 2 yr) and 17 healthy matched control subjects were studied during a 75 km cross-country skiing race. Blood samples were taken before and immediately after exercise, and also during the ski race. RESULTS: During the semitriathlon race, serum insulin, C-peptide, glucagon cortisol, growth hormone ACTH, prolactin, and plasma renin activity increased two- to ninefold, whereas serum testosterone fell. Apart from a fall in magnesium, serum electrolyte concentrations remained unchanged. Before long-term skiing, patients reduced their insulin dose by 30-40%. They were hyperglycemic during the initial part of the race, but near normoglycemic thereafter. There were large interindividual variations in the increments of counterregulatory hormones, whereas serum testosterone and luteinizing hormone fell quite uniformly. Plasma renin activity and aldosterone concentrations rose similarly in diabetic and healthy subjects, whereas the rise in antidiuretic hormone was slightly greater in diabetic patients. During the initial part of the race, serum atrial natriuretic peptide fell in both groups. CONCLUSIONS: Severalfold increments in hormone concentrations contribute to the maintenance of fuel and fluid homeostasis during long-term exercise. With an appropriate adjustment of insulin dose and diet, also type I diabetic patients can participate in competitive long-term exercise.

Adult↗
PubMed1991

Is the treatment of metastatic carcinoid tumor with interferon not as successful as suggested?

Eight patients with metastatic carcinoid tumor, seven of whom had symptoms of the carcinoid syndrome, were treated with either human leukocyte interferon (seven patients) or recombinant alpha-interferon (IFN alpha-2b) (one patient) at doses of 4.5 to 21 x 10(6) IU weekly for 1 to 21 (mean, 8.5) months. Tumor regression on computed tomography (CT) scan was found in one patient, the CT findings remained unchanged in three, and the tumor progressed in four patients. A clearcut and continuing decrease in urinary levels of 5-hydroxyindoleacetic acid (5-HIAA) was observed in one patient and a transient one in four patients. The symptoms improved in only two of seven patients. Four patients had leukopenia develop, which was circumvented by reducing the dose. The authors conclude that interferon therapy of the carcinoid tumor is not as successful as has been suggested in previous reports.

Adult↗
PubMed1991

Obstructive sleep apnoea syndrome in morbidly obese patients.

Twenty-seven morbidly obese patients (13 men and 14 women) with body mass index greater than or equal to 40 kg m-2 were examined. The mean age of the subjects was 36.9 +/- 8.2 years (range 23-51 years), and the mean BMI was 50.2 +/- 6.2 kg m-2 (range 40.0-62.9 kg m-2). A whole-night sleep recording was made for all patients with signs or symptoms indicative of possible obstructive sleep apnoea syndrome (OSAS). If the first nocturnal sleep recording was abnormal, it was controlled after 1 year. Eleven (10 men and one woman) of the 27 patients had an oxygen desaturation index (ODI) of 10 h-1. They were symptomatic with excessive daytime sleepiness or other daytime symptoms of OSAS. The occurrence of OSAS in men and women was 76.9 and 7.1%, respectively. Arterial hypertension was associated with OSAS, but not with smoking or the degree of obesity. Antihypertensive treatment was received by nine of the 27 patients; six of them had OSAS. Thus six of the 11 (54.5%) patients with OSAS and three of the 16 (18.8%) nonapnoeic patients were treated for arterial hypertension (Fisher exact test, P = 0.042). The odds ratio of OSAS for arterial hypertension is 5.2 (95% CI, 0.71-43.6). Vertical-banded gastroplasty was performed in 14 patients, three of whom had OSAS. The selection of patients for gastroplasty was made without taking into account the results of sleep recordings. In the three OSAS patients, a 30-38% reduction in BMI was achieved by surgery. Eight patients with OSAS were treated with an intensified dietary regimen, and the reduction in BMI ranged from -2.6 to 33%. OSAS was either cured or significantly improved in six (55%) patients, with a mean reduction in BMI of 27%, while in patients with persistent OSAS the mean reduction in BMI was only 7%.

Adult↗
PubMed1991

Insulin therapy in maturity-onset diabetes.

A prime target of insulin action in patients with maturity onset diabetes is suppression of hepatic glucose production in both the fasting and postprandial states. In patients who fail to respond to oral treatment insulin improves glycaemic control, has an antiatherogenic effect on the serum lipoprotein pattern, and increases well being. The beneficial long-term effects of insulin therapy on morbidity and mortality are, however, still unproved. The regimens of insulin therapy are not established. In patients with normal or increased basal serum C-peptide concentration treatment may start with intermediate or long-acting insulin at bedtime together with oral medication, or in the morning with or without oral medication. If this fails two injections of intermediate-acting insulin or multiple injections of short-acting insulin should be started. Hypoglycaemia is uncommon in maturity onset diabetes treated with insulin, but moderate weight gain usually occurs. The possible role of hyperinsulinemia as a predisposing factor for atherogenesis remains unresolved. Despite controversies over treatment, any patient with maturity onset diabetes not responding to oral agents should be regarded as a candidate for insulin therapy.

Diabetes Mellitus, Type 2↗