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Results for “Glucose Intolerance”

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PubMed1991

Inverse association between fish intake and risk of glucose intolerance in normoglycemic elderly men and women.

OBJECTIVE: To examine the association of fish intake with the subsequent risk of impaired glucose tolerance and diabetes mellitus (glucose intolerance). RESEARCH DESIGN AND METHODS: In 1971, information about food intake was obtained by the cross-check dietary history method on 175 men and women aged 64-87 yr who were normoglycemic and free of clinical diabetes. During the follow-up period from 1972 to 1975, an oral glucose tolerance test was performed annually, and in 59 of 175 elderly people a diagnosis of glucose intolerance was made at least once. RESULTS: In 1971, approximately 60% of the subjects usually ate fish, with a mean daily intake of 24.2 g. In fish eaters, the incidence of glucose intolerance was significantly lower compared with nonfish eaters (odds ratio [OR] 0.40, 95% confidence interval [CI] 0.21-0.77). With logistic regression analysis, this inverse association could not be explained by taking into account age and sex or possible confounding baseline characteristics, such as the prevalence of myocardial infarction, body mass index, energy intake per kilogram body weight, or intake of carbohydrates (OR 0.47, 95% CI 0.23-0.93). Baseline characteristics of the oral glucose tolerance test and serum triglyceride levels could also not account for this result. CONCLUSIONS: These results suggest that, in an elderly population, the habitual consumption of a small amount of fish may protect against the development of impaired glucose tolerance and diabetes mellitus.

Aged↗

PubMed2001

Glucose intolerance is predicted by the high Fasting Insulin-to-Glucose ratio.

OBJECTIVE: To determine whether impaired glucose tolerance (IGT) is predicted by high Fasting Insulin-to-Glucose (FIG) ratio and to establish its correlation with insulin resistance and fasting insulin. MATERIAL AND METHODS: A population-based three-year follow-up study was performed. The target population consisted of healthy volunteers, men and non-pregnant women aged 30 years or over. Participants were required to have normal referenced ranges of OGTT and blood pressure. Previous diagnosis of chronic diseases was an exclusion criterion. At baseline and at the 3-yr of follow-up, an OGTT was performed. The ratio of serum Fasting Insulin (microUI/ml)/Fasting Glucose (mg/dl) was used to calculate the FIG ratio. Insulin action and secretion were estimated by HOMA and Insulinogenic index, respectively. RESULTS: The FIG ratio was directly correlated with the HOMA index (r=0.83, p<0.01) and fasting insulin (r=0.95, p<0.001). Multivariate logistic regression analysis showed that IGT was more likely to develop in subjects with high FIG ratio (RR 5.01; CI(95%) 1.9-12.2, p=0.02), high HOMA index (RR 6.1; CI(95%) 2.1-11.1, p=0.01), and fasting hyperinsulinemia (RR 4.7 CI(95%) 2.7-13.2, p<0.05). The cutoff point of FIG ratio for determining the risk of developing IGT was 0.25 +/- 0.05. CONCLUSIONS: The FIG ratio could be a reliable alternative for the screening of apparently healthy subjects in high risk groups.

Adult↗

PubMedDate not supplied

Risk factors associated with persistence of glucose intolerance one year after gestational diabetes.

One hundred and fourteen women, 89 with previous gestational diabetes and 25 who showed a normal glucose tolerance during pregnancy were retested by OGTT one year postpartum. Gestational diabetics were divided into two groups according to the severity of glucose intolerance. 97.6% of mild gestational diabetics and 79.2% of severe cases returned to normality postpartum. A different behaviour of these groups was shown by comparing OGTT areas before and after delivery. Body Mass Index and the degree of severity of glucose intolerance were shown to be predictive for the persistence of the abnormality postpartum. Follow-up for three to four years was continued in 8 cases of previous severe gestational diabetes. In seven of them a glucose intolerance appeared again during the follow-up after the temporary improvement one year after delivery.

Adult↗

PubMed2004

Ingestion of guar gum hydrolysate, a soluble and fermentable nondigestible saccharide, improves glucose intolerance and prevents hypertriglyceridemia in rats fed fructose.

Fructose feeding provides a dietary model of insulin resistance accompanied by hypertriglyceridemia. We examined the effects of guar gum hydrolysate (GGH), a soluble and fermentable nondigestible saccharide with low viscosity, on glucose intolerance and hypertriglyceridemia in rats fed high-fructose diets. Rats were fed either a dextrin-based or a fructose-based diet with or without GGH (75 g/kg) for 30 d. Oral glucose tolerance tests (OGTTs) were performed 0, 14, and 28 d after feeding. High-fructose feeding negatively affected glucose tolerance on d 14 and 28. The addition of GGH to the diets improved glucose intolerance on d 28. Fructose feeding induced hyperinsulinemia after an oral glucose load; this was also improved by GGH on d 28. The glycogen concentration in the gastrocnemius muscles of rats was lowered by dietary fructose, and GGH supplementation abolished this decrease. Triglycerides in the plasma and livers of rats fed fructose diets were elevated, and the increases were ameliorated by supplemental GGH. Regardless of the type of carbohydrate, GGH enlarged the cecum and increased the cecal SCFA pools. In conclusion, supplemental feeding of GGH to rats improved the glucose intolerance and hypertriglyceridemia induced by a high-fructose diet. Possible mediators of these beneficial effects of GGH are the SCFAs produced by microbial fermentation of GGH in the large intestine.

Animals↗

PubMed1994

Roles of insulin resistance and beta-cell dysfunction in the pathogenesis of glucose intolerance in cystic fibrosis.

The roles of insulin deficiency and insulin resistance in the pathogenesis of glucose intolerance in cystic fibrosis (CF) were evaluated in eight patients (aged 16.5 +/- 1.9 yr), four with normal glucose tolerance (NGT) and four with impaired glucose tolerance (IGT), and in seven healthy control (CN) subjects. First and second phase insulin secretions were evaluated during a hyperglycemic clamp. Hepatic glucose production (HGP) and insulin-stimulated glucose disposal were measured using [6,6-2H2]glucose and a stepwise hyperinsulinemic-euglycemic clamp. First and second phase insulin levels were significantly lower in both groups of CF patients compared with control values. There was an inverse relationship between glycohemoglobin level and first phase insulin (r = -0.81; P = 0.015) and second phase insulin (r = -0.97; P < 0.001). During the hyperglycemic clamp, the insulin sensitivity index was lower in CF-IGT, but not CF-NGT, compared with control values (6.66 +/- 1.79, 12.82 +/- 1.61, and 13.02 +/- 1.78 mumol/kg.min/pmol.L, respectively; P < 0.05). Basal HGP and fasting plasma glucose were higher in CF vs. CN [24.8 +/- 2.9 vs. 16.9 +/- 1.4 mumol/kg.min (P = 0.036) and 5.8 +/- 0.2 vs. 5.4 +/- 0.1 mmol/L (P = 0.035), respectively]. During the hyperinsulinemic euglycemic clamp, insulin-stimulated glucose disposal was significantly lower in CF-IGT (45.68 +/- 4.87 mumol/kg.min) vs. CF-NGT (78.99 +/- 1.34 mumol/kg.min) and CN (71.74 +/- 6.88 mumol/kg.min). Insulin sensitivity was lower in CF-IGT vs. CF-NGT (7.04 +/- 0.86 and 14.38 +/- 0.84 mumol/kg.min/pmol.L; P < 0.05). We conclude that 1) glycohemoglobin is a strong correlate of insulin deficiency in CF; and 2) glucose intolerance in this group of CF patients occurred as a consequence of concomitant insulin deficiency and insulin resistance.

Adolescent↗

PubMed2002

A quantitative trait locus that accounts for glucose intolerance maps to chromosome 8 in hereditary obese KK-A(y) mice.

KK and KK-A(y) mice serve as animal models of non-insulin-dependent diabetes mellitus with moderate obesity. Quantitative trait locus (QTL) analysis was performed to identify gene loci that account for fasting hyperglycemia, glucose intolerance and plasma insulin in 91 F(2) females of a C57BL/6JxKK-A(y) intercross. For glucose intolerance, a significant QTL was identified on chromosome 8, with a maximum lod score of 5.6. This locus had strong influence on the late phase of the intraperitoneal glucose tolerance test (IPGTT), suggesting that the locus may have role in glucose clearance rather than in mere hyperglycemia. In addition, three suggestive QTLs were identified on chromosomes 1 (fasting glucose), 3 (fasting insulin) and 4, (blood glucose at 120 min during IPGTT, and glucose intolerance).

Animals↗

PubMed2006

Development of cookie test for the simultaneous determination of glucose intolerance, hyperinsulinemia, insulin resistance and postprandial dyslipidemia.

A new cookie test was developed for the simultaneous evaluation of multiple risk factors such as glucose intolerance, hyperinsulinemia, insulin resistance and postprandial dyslipidemia. The cookie consisting of 75 g carbohydrate and 25 g fat is ingested and the blood samples are obtained at 0, 1 and 2 hours later. When the two carbohydrate sources, liquid glucose and test cookie, were compared as a glucose load within 3 months, the 2 hr plasma glucose levels were not statistically different, proposing the use of the same criteria at 2 hour glucose level for the diagnosis of diabetes and impaired glucose tolerance (IGT) in subjects without exocrine pancreatic dysfunction. In addition, hyperinsulinemia, insulin resistance (AUC insulin, and/or AUC insulin X AUC glucose), and postprandial hyperlipidemia (DeltaTG, Triglyceride; DeltaRLP, remnant like particles) have been simultaneously uncovered. Reactive hypoglycemia with adverse epigastric discomfort was observed in 26.3% of the control subjects with liquid glucose, while it was observed in only 1 case (5.3%) without any symptom with cookie tests. In fact, one reactive hypoglycemia out of 5 with liquid glucose turned out to be IGT with cookie test. In 64 subjects with lifestyle-related diseases, cookie test revealed hyperinsulinemia and insulin resistance in 56% respectively, postprandial hyperlipidemia in 39%, diabetes and IGT in 22-23% of each of the subjects and all showed at least one abnormal value. In contrast, in university students with exercise habit, all showed normal results with cookie test. In addition, improved insulin sensitivity over non-exercise group was obverved. In summary, the cookie test provided more informations compared with OGTT using liquid glucose and with fewer side effects. Simultaneous evaluation of glucose intolerance, hyperinsulinemia, insulin resistance, and postprandial hyperlipidemia was also possible.

Adult↗

PubMed1986

Effects of obesity, hyperinsulinemia, and glucose intolerance on insulin action in adipose tissue of sixty-year-old men.

The relative effects of obesity alone, and in combination with fasting hyperinsulinemia and glucose intolerance, on the peripheral action of insulin in adipose tissue were investigated in twenty-four 60-yr-old men, who had been followed for 10 yr. They were divided into four groups of six subjects each on the basis of the following criteria: (1) normal body weight, normal fasting insulin level, and normal glucose tolerance; (2) moderate obesity, normal fasting insulin level, and normal glucose tolerance; (3) moderate obesity, fasting hyperinsulinemia, and normal glucose tolerance; and (4) moderate obesity, fasting hyperinsulinemia, and newly developed, moderate, untreated fasting hyperglycemia and/or glucose intolerance (i.e., mild type II diabetes mellitus). Specific adipocyte insulin binding and the effects of the hormone on adipose tissue lipolysis and glucose oxidation were determined. Insulin receptor binding per cell and per cell surface area were similar in all four groups. Regarding antilipolysis, the insulin sensitivity was the same in all groups and the maximum effect was significantly increased in the three obese groups, as compared with the normal-weight control group. In groups 1-3, insulin stimulated adipose tissue glucose oxidation in a dose-dependent way, and the sensitivity and responsiveness to insulin were comparable. In contrast, in the obese glucose-intolerant subjects (4) there was no significant effect of insulin on glucose oxidation when the hormone was added in increasing concentrations of less than or equal to 35 nmol/L. The basal glucose oxidation was similar in all four study groups. The in vivo insulin tolerance was gradually reduced in groups 2-4, as compared with the normal-weight control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

PubMed1993

Glucose intolerance as a consequence of oral terbutaline treatment for preterm labor.

BACKGROUND: In this case series, glucose regulation is examined prospectively during treatment with terbutaline sulfate for premature labor in women who were (1) previously documented as nondiabetic, (2) found to have gestational diabetes mellitus (GDM), and (3) tested for glucose intolerance while terbutaline was being administered. The glucose profiles of women treated with terbutaline were contrasted with the profiles of nondiabetic women and women known to have GDM who were not in premature labor. METHODS: Subjects tested capillary blood glucose an average of five times a day during terbutaline treatment and for 1 week after terbutaline treatment was discontinued. They used memory-based reflectometers that stored and transmitted self-monitored blood glucose data to a personal computer. RESULTS: A significant difference (P = .001) was found between average fasting glucose values (111 +/- 23 mg/dL) for the five nondiabetic subjects treated with terbutaline and values of patients in an historical control group (41 nondiabetic pregnancies [72 +/- 22 mg/dL]) who were not in premature labor. The four diabetic subjects and the one subject who had not been previously tested also experienced higher blood glucose levels during tocolytic therapy. Glucose levels returned to preintervention values with the cessation of terbutaline therapy. CONCLUSIONS: It has been previously suggested that terbutaline increases hepatic glycogenolysis, which may aggravate glucose intolerance. This phenomenon, combined with normal pregnancy-induced insulin resistance, may explain abnormal ambulatory glucose patterns in women who are euglycemic before introduction of terbutaline therapy.

Adult↗

PubMed1981

[Serum prolactin in obese subjects with and without glucose intolerance].

Basal values of H-Prl have been assayed with reproducible RIA in two accurately selected group of subjects: 1) obese with latent glucose intolerance; 2) obese without glucose intolerance. In these patients have been valued also IRI and blood glucose (GOD-POD Biochemia). The data reported in this paper show that therein't correlation between basal H-Prl values and difference obese -- normal of IRI concentrations neither in non-diabetics nor in pre-diabetics obese. It indicate that the H-Prl not plays a controinsular role in obese-prediabetics subjects. No difference in basal values of H-Prl we found in the examined patient obese pre- and not-diabetics.

Adolescent↗

PubMed1999

Impact of the 1997 American Diabetes Association criteria on classification of glucose intolerance among Kuwaitis below 50 years of age.

Type 2 (non-insulin-dependent) diabetes is emerging as a leading chronic non-communicable disease among the adult Kuwaiti population. Based on the World Health Organization and similar reports the projected estimates for subjects suffering from type 2 diabetes by the years 2000 and 2010 show a striking tendency to high rates of the disease in our area. We report the prevalence rates of glucose intolerance among a relatively young adult Kuwaiti population below 50 years of age and the effect of implementing the recent 1997 American Diabetes Association diagnostic criteria on the frequency of type 2 diabetes, impaired glucose tolerance and impaired fasting glucose among this group. The overall prevalence rate for the three categories of glucose intolerance reached as high as 15.8% (95% CI, 14.2 to 17.4). Age, though all subjects were below 50 years, parental history of type 2 diabetes, diastolic blood pressure and serum triglycerides were found to be significant associated risk factors for the development of type 2 diabetes. Obesity was an apparent significant factor associated with the three forms of glucose intolerance (p < 0.001). Obesity and physical inactivity were documented in both non-diabetic and more so in diabetic Kuwaiti adults, which should form the basis of any immediate intervention programme. An integrated approach to the prevention of the described critical risk factors associated with type 2 diabetes is highly recommended in Kuwait. Research, focused on genetics of type 2 diabetes in the highly susceptible Kuwaiti population, should be planned.

Adult↗

PubMed2001

[Prevalence of type 2 diabetes mellitus and glucose intolerance in the Setif area (Algeria)].

OBJECTIVE: Diabetes mellitus stands as a major public health issue in Algeria and has an important socioeconomical impact. Our study involved a representative sample of 1457 subjects and aimed at assessing the prevalence of type 2 diabetes and glucose intolerance in the population of Setif Wilaya, aged between 30 and 64 years old. MATERIAL AND METHODS: Diagnosis was based on oral glucose tolerance test, according to World Health Organisation criteria. RESULTS: Diabetes prevalence was 8.2% (CI: 95%: 6.8% to 9.6%). It increased with age, while 50% of cases were undiagnosed, without any difference according to sex nor urban (7.3%)/rural (9.7%) distribution. Glucose intolerance prevalence was 7.1 (CI 95%: 5,8% to 8,4%). Age-standardized prevalence, according to world population data provided by WHO, was 9.08% for diabetes and 7.5% for glucose intolerance. When the new American Diabetes Association Criteria were used, prevalence of type 2 diabetes was 8.8 (CI: 95%: 7.3% to 10.2%) and that of fasting hyperglycemia was 6.9% (CI: 95%: 5.6 to 8.2). According to these new criteria, among the 66 cases with undiagnosed diabetes, 79% presented with a fasting blood glucose > or =126 mg/dl. CONCLUSION: This relatively high diabetes prevalence calls for an appropriate management and health education, particularly focused on high risk subjects. These results bring the the first detailed prevalence data in an Algerian population.

Adult↗

PubMed1998

Marked hyperleptinemia after high-fat diet associated with severe glucose intolerance in mice.

We asked whether the likelihood for mice of the C57BL/6J strain to develop glucose intolerance when fed a high-fat diet is related to the increase in circulating levels of leptin or free fatty acids (FFA). We therefore administered a high-fat diet (58% fat) or a control diet (11% fat) for 1.5 years. NMRI mice were used as a more glucose-tolerant control group. After a high-fat diet, the area under the glucose curve following an intraperitoneal glucose challenge (1 g/kg) increased more markedly in C57BL/6J mice (by 42+/-8%) than in NMRI mice (by 21+/-3%, P = 0.007). Plasma levels of insulin, leptin and FFA increased in both strains of mice, whereas plasma glucose levels were elevated after the high-fat diet only in C57BL/6J mice. The slope of the relationship between body weight and plasma leptin was higher in C57BL/6J mice than in NMRI mice. suggesting leptin insensitivity. Circulating leptin correlated to circulating insulin in both strains of mice, whereas plasma FFA correlated to plasma insulin in NMRI mice but not in C57BL/6J mice. These correlations remained significant after adjustment for body weight. The results show that elevated leptin and FFA levels evolve after high-fat feeding in mice, in conjunction with evolvement of glucose intolerance and hyperglycemia.

Animals↗

PubMed1994

Glucose intolerance as a predictor of hypertension in pregnancy.

Insulin resistance is associated with and may be causal in essential hypertension, but the relation between insulin resistance and hypertension arising de novo in pregnancy is unclear. Transient hypertension of pregnancy (new-onset nonproteinuric hypertension of late pregnancy) is associated with a high risk of later essential hypertension and thus may have similar pathophysiology. To assess the association between glucose intolerance and subsequent development of proteinuric and nonproteinuric hypertension in pregnancy in women without underlying essential hypertension or overt glucose intolerance, we performed a retrospective case-control study comparing glucose levels on routine screening for gestational diabetes mellitus among women subsequently developing hypertension. Women who developed hypertension in pregnancy (n = 97) had significantly higher glucose levels on 50-g oral glucose loading test (P < .01) and a significantly higher frequency of abnormal glucose loading tests (> or = 7.8 mmol/L) (P < .01) than women who remained normotensive (n = 77). Relative glucose intolerance was particularly common in women who developed nonproteinuric hypertension. Women who developed hypertension also had greater prepregnancy body mass index (P < or = .0001) and baseline systolic and diastolic blood pressures (P < or = .0001 for both), although all subjects were normotensive at baseline by study design. However, after adjustment for these and other potential confounders, an abnormal glucose loading test remained a significant predictor of development of hypertension (P < .05) and, specifically, nonproteinuric hypertension in pregnancy (P < .01). Among a subgroup of women in whom insulin levels were also measured (n = 80), there was a nonsignificant trend toward higher insulin levels in women developing hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗

PubMed1999

Chronic ventromedial hypothalamic infusion of norepinephrine and serotonin promotes insulin resistance and glucose intolerance.

The ventromedial hypothalamus (VMH) is involved in the regulation of peripheral metabolism. We and others have shown that activities, or extracellular metabolites of norepinephrine (NE) and serotonin (5-HT) are elevated in the VMH of both genetically and seasonally insulin-resistant and glucose-intolerant animals. This study examined whether chronic increases in VMH NE and 5-HT concentration of normal animals might lead to insulin-resistant and glucose-intolerant conditions in hamsters. Euinsulinemic, glucose-tolerant hamsters were infused continuously for 5 weeks into the right VMH with either vehicle, NE (5 or 25 nmol/h), 5-HT (2.5 nmol/h), or NE (5 or 25 nmol/h) plus 5-HT (2.5 nmol/h) through osmotic minipumps. Compared to vehicle, NE (25 nmol/h) significantly increased the glucose total area under the curve (TAUC) by 32% during glucose tolerance tests (GTT) conducted after 5 weeks' infusion. 5-HT alone significantly increased the GTT insulin TAUC (131%) and basal plasma insulin level (116%) but not glucose TAUC. NE (5 nmol/h) plus 5-HT infusion significantly increased insulin TAUC (129%) and basal plasma insulin (120%), whereas NE (25 nmol/h) plus 5-HT infusion significantly increased both the GTT glucose and insulin TAUC (43 and 113%, respectively), as well as basal plasma insulin level (158%), relative to vehicle infusion. Our findings demonstrate for the first time the differential and, more importantly, interactive effects of increased VMH NE and 5-HT in producing hyperinsulinemia, insulin resistance and glucose intolerance.

Animals↗

PubMed2006

Glucose intolerance in Japanese patients with polycystic ovary syndrome.

BACKGROUND: Hyperinsulinemia, which is related to obesity, played a pathogenic role in polycystic ovary syndrome (PCOS). However, the incidence of obesity in Japanese women with PCOS is different from that reported in patients with PCOS in Europe and USA. We should determine if insulin resistance occurs in Japanese PCOS. The purpose of this study is to assess the presence of insulin resistance in Japanese PCOS, while also considering obesity as a factor. METHODS: We divided the patients with polycystic ovary (PCO) into three groups based on body mass index and levels of gonadotropin. Nine obese PCOS, 34 normal body-weighted PCOS (luteinizing hormone (LH)/follicle stimulating hormone (FSH) >1.0) and 11 normal LH (LH/FSH </= 1.0), normal body-weighted PCO were studied. We compared those patients to 16 control subjects with normal ovulation or with hypothalamic anovulation. Eleven women in the control were normal body-weighted and five were obese. Patients were given an oral glucose tolerance test. Testosterone, plasma glucose and serum immunoreactive insulin after oral administration of 75 g dextrose were studied. We also compared glucose-intolerance [total plasma glucose (SigmaPG) and insulin (SigmaIRI), insulinogenic index (I.I.), fasting plasma glucose/immunoreactive insulin (FPG/IRI), homeostasis model assessment of insulin resistance (HOMA-R)] and testosterone among these groups. RESULTS: There were no differences in SigmaPG, SigmaIRI, I.I., FPG/IRI or HOMA-R between PCOS and controls. However, there were significant differences in SigmaPG, SigmaIRI, FPG/IRI and HOMA-R between obese and normal body-weighted patients. Similarly, there were no differences in SigmaPG, SigmaIRI, I.I., FPG/IRI or HOMA-R between PCOS and controls in the normal body-weighted group. However, there were significant differences in SigmaPG, SigmaIRI, FPG/IRI and HOMA-R between the obese and the normal body-weighted PCOS. There were also significant differences in SigmaPG and I.I. between LH-dominant, normal body-weighted PCOS and normal LH PCO. CONCLUSION: Japanese PCOS might have insulin-resistance but the factor of obesity had a stronger effect on insulin-resistance than did the existence of PCOS. The possibility of a different type of glucose-intolerance was suggested in the patients with ultrasonographical PCO in whom gonadotropin secretion was abnormal.

Adolescent↗

PubMed1989

Normal insulin sensitivity during the phase of glucose intolerance but insulin resistance at the onset of diabetes in the spontaneously diabetic BB rat.

In diabetes-prone BB rats, 30 to 50% of animals undergo autoimmune destruction of the pancreatic B-cells leading to a short period of glucose intolerance, followed by an abrupt onset of diabetes. We have examined whether the glucose intolerance period and the onset of diabetes are associated with changes in insulin sensitivity, using the euglycaemic hyperinsulinaemic clamp coupled with [3-3H] glucose infusion. Glucose intolerant rats were detected by a transient glycosuria one hour after an oral glucose load performed every four days. Insulin sensitivity studied in these rats the day following their detection was normal. Other diabetes-prone BB rats were tested daily and studied on the first day of glycosuria. In the basal state, glucose production was increased in diabetic rats (11.3 +/- 1.1 vs 7.1 +/- 0.8 mg.min-1.kg-1, p less than 0.05). Tissue glucose utilization was similar in diabetic and control rats (8.3 +/- 0.5 vs 7.1 +/- 0.8 mg.min-1.kg-1) despite a three fold higher glycaemia in the diabetic rats. During the hyperinsulinaemic clamps, glycaemia was clamped at 6.1-6.6 mmol/l in diabetic and control rats. A decreased insulin sensitivity was observed in diabetic rats at submaximal (200 microU/ml) and maximal (1500 microU/ml) insulin concentrations for both inhibition of hepatic glucose production and stimulation of glucose utilization. No autoantibodies against insulin could be detected in the plasma of diabetic rats. Plasma concentrations of glucagon, catecholamines, ketone bodies and fatty acids were similar in control and diabetic rats during the clamp studies.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗

PubMed2006

Suppressive effects of diacylglycerol oil on postprandial hyperlipidemia in insulin resistance and glucose intolerance.

The diacylglycerol (DAG), a commonly used as a cooking oil in Japan, results in a lower elevation of serum triglyceride (TG) after ingestion compared to triacylglycerol (TAG). Postprandial hyperlipidemia (PPHL) and an increase in remnant lipoproteins (RLP) levels are risk factors for CAD, and a close relationship between PPHL and type 2 diabetes and/or insulin resistance has been reported. To evaluate the effect of DAG on PPHL in insulin resistance and glucose intolerance, 11 subjects with a normal glucose tolerance (NGT) and 14 subjects with IGT received oral fat tolerance test (OFTT) twice. They ingested emulsified test oils prepared with either DAG or TAG. In the IGT subjects, after the DAG and TAG load, the serum concentrations of TG, RLP-TG, and RLP-cholesterol increased throughout the 4-h study. The responses of these variables above baseline after the DAG load were significantly smaller than those after the TAG load (p<0.05). In contrast, in the NGT subjects, changes in these parameters were much smaller than those observed for IGT subjects. The difference in the integrated responses for serum RLP-cholesterol concentration during OFTT between DAG and TAG in all subjects can be easily explained by the integrated response of insulin rather than glucose during oral glucose tolerance test (r=0.7, p<0.01). DAG was more effective in insulin resistant and hyperinsulinemic participants regardless of glucose intolerance, and may be beneficial in reducing the extent of CAD risk in such individuals.

Adult↗