Biomedical subjects

A Nadeau

Publications and source records attributed to A Nadeau.

At least 55 records · Page 3Linked to original sources

PubMed1997

Abdominal visceral fat is associated with a BclI restriction fragment length polymorphism at the glucocorticoid receptor gene locus.

Several investigations have suggested that body fat distribution is influenced by nonpathologic variations in the responsiveness to cortisol. Genetic variations in the glucocorticoid receptor (GRL) could therefore potentially have an impact on the level of abdominal fat. A restriction fragment length polymorphism (RFLP) has previously been detected with the BclI restriction enzyme in the GRL gene identifying two alleles with fragment lengths of 4.5 and 2.3 kb. This study investigates whether abdominal fat areas measured by computerized tomography (CT) are associated with this polymorphism in 152 middle-aged men and women. The less frequent 4.5-kb allele was found to be associated with a higher abdominal visceral fat (AVF) area independently of total body fat mass (4.5/4.5 vs. 2.3/2.3 kb genotype; men: 190.7 +/- 30.1 vs. 150.7 +/- 33.3 cm2, p = 0.04; women: 132.7 +/- 37.3 vs. 101.3 +/- 34.5 cm2, p = 0.06). However, the association with AVF was seen only in subjects of the lower tertile of the percent body fat level. In these subjects, the polymorphism was found to account for 41% (p = 0.003) and 35% (p = 0.007), in men and women, respectively, of the total variance in AVF area. The consistent association between the GRL polymorphism detected with BclI and AVF area suggests that this gene or a locus in linkage disequilibrium with the BclI restriction site may contribute to the accumulation of AVF.

Abdomen↗

PubMed1997

Suggestive linkages between markers on human 1p32-p22 and body fat and insulin levels in the Quebec Family Study.

A single-gene rodent mutation (diabetes) and a quantitative trait locus (dietary obese 1) mapped to the mid portion of mouse chromosome 4 have been related to obesity and/or insulin levels. Synteny relationships place their putative human homologs on 1p31 and 1p35-p31, respectively. In 137 sibships of adult brothers and sisters from the Québec Family Study, genetic linkages between seven microsatellite markers from 1p32-p22 and various obesity- and diabetes-related quantitative phenotypes were examined using single locus sibpair linkage analysis. Suggestive linkages were observed between markers D1S476 and body mass index (p = 0.05), fat mass (p = 0.02), the sum of six skinfolds (p = 0.02), the insulin area after an oral glucose tolerance test (p = 0.02), and between the neighboring marker D1S200 and body mass index (p = 0.03), and fat mass (p = 0.009). Suggestive linkages were also observed between the more telomeric markers D1S193 and body mass index (p = 0.03), and between the neighboring marker D1S197 and fasting insulin level (p = 0.05). No linkage was observed with the trunk to extremity skinfolds ratio. These linkages suggest that human homologs of the mouse diabetes or dietary obese 1 and/or other genes in this interval on chromosome 1 play a role in the regulation of body mass, body composition, and insulin levels, but not of subcutaneous fat distribution.

Adolescent↗

PubMed1997

Regional variation in adipose tissue insulin action and GLUT4 glucose transporter expression in severely obese premenopausal women.

Insulin action and GLUT4 expression were examined in adipose tissue of severely obese premenopausal women undergoing gastrointestinal surgery. Fat samples were taken from three different anatomical regions: the subcutaneous abdominal site, the round ligament (deep abdominal properitoneal fat), and the greater omentum (deep abdominal intraperitoneal fat). The stimulatory effect of insulin on glucose transport and the ability of the hormone to inhibit lipolysis were determined in adipocytes isolated from these three adipose depots. Insulin stimulated glucose transport 2-3 times over basal rates in all adipocytes. However, round ligament adipose cells showed a significantly greater responsiveness to insulin when compared to subcutaneous and omental adipocytes. Round ligament fat cells also displayed the greatest sensitivity and maximal antilipolytic response to insulin. We also investigated whether regional differences in fat cell insulin-stimulated glucose transport were linked to a differential expression of the GLUT4 glucose transporter. GLUT4 protein content in total membranes was 5 and 2.2 times greater in round ligament adipose tissue than in subcutaneous and omental fat depots, respectively. Moreover, GLUT4 mRNA levels were 2.1 and 3 times higher in round ligament than in subcutaneous or omental adipose tissues, respectively. Adipose tissue GLUT4 protein content was strongly and negatively associated (r = -0.79 to -0.89, p < 0.01) with the waist-to-hip ratio but not with total adiposity. In conclusion, these results demonstrate the existence of site differences in adipose tissue insulin action in morbidly obese women. The greater insulin effect on glucose transport in round ligament adipocytes was associated with a higher expression of GLUT4 when compared to subcutaneous abdominal and omental fat cells. Moreover, despite the regional variation in GLUT4 expression, an increased proportion of abdominal fat was found to be associated with lower levels of GLUT4 in all adipose regions investigated.

Adipocytes↗

PubMed1997

Plasma leptin concentrations: gender differences and associations with metabolic risk factors for cardiovascular disease.

The cloning of the obese gene and the characterization of its protein product, leptin, has permitted the study of a new hormone potentially involved in the regulation of adipose tissue mass. The present study examined the gender differences in fasting plasma leptin concentration and its relationship to body fatness, adipose tissue distribution and the metabolic profile in samples of 91 men (mean age +/- SD: 37.3 +/- 4.8 years) and 48 women (38.5 +/- 6.8 years). Plasma leptin concentrations were strongly associated with body fat mass measured by underwater weighing [men: r = 0.80, p < 0.0001; women: r = 0.85, p < 0.0001]. In both genders, plasma leptin levels were also strongly correlated with waist girth as well as cross-sectional areas of abdominal subcutaneous and visceral adipose tissue measured by computed tomography. Women had, on average, plasma leptin concentrations that were three times higher than men. Furthermore, this gender difference remained significant when comparing men and women matched for similar levels of body fat mass. The associations between plasma leptin and lipoprotein concentrations were dependent of adiposity. In both men and women, elevated fasting plasma leptin levels were associated with higher plasma insulin concentrations, but only in women was the association maintained after correction for fat mass. Thus, results of the present study show that women have higher plasma leptin levels compared to men, independent of the concomitant variation in total body fat mass. Furthermore, our results also suggest that, in women, the association between plasma leptin and insulin concentrations is independent of adiposity, a finding which provides further support to the observation that adipose tissue leptin secretion may be upregulated by insulin.

Adipose Tissue↗

PubMed1997

Relationships between endogenous steroid hormone, sex hormone-binding globulin and lipoprotein levels in men: contribution of visceral obesity, insulin levels and other metabolic variables.

Excess visceral adipose tissue (AT) and hyperinsulinemia are important correlates of an altered lipoprotein profile. It has also been reported that testosterone, adrenal C19 steroids and sex hormone-binding globulin (SHBG) concentrations are associated with plasma lipoprotein levels. The aim of the present study was to investigate the relative contributions of endogenous steroid hormone and SHBG levels, of visceral AT accumulation measured by computed tomography, and of fasting insulin and free fatty acid (FFA) concentrations to the variation of plasma lipoprotein levels in men. For this purpose, plasma concentrations of testosterone, dehydroepiandrosterone (DHEA), androstene-3beta,17beta-diol (delta5-DIOL), androstenedione (delta4-DIONE), estrone and estradiol, as well as SHBG levels were determined in a sample of 76 men covering a wide range of body fatness values. Higher testosterone levels were associated with a more favorable lipoprotein profile as it showed significant correlations with triglyceride (TG), total cholesterol and LDL-cholesterol (LDL-C) concentrations (r= -0.25, -0.25 and -0.27, respectively; P < 0.05). Higher plasma adrenal C19 steroid levels were also associated with a favorable lipoprotein profile as DHEA, delta4-DIONE and delta5-DIOL levels were negatively correlated with total cholesterol (r = -0.24, -0.33 and -0.24, respectively; P < 0.05) and LDL-C (r = -0.23, -0.31 and -0.28, respectively; P < 0.05). SHBG levels were negatively correlated with TG concentrations (r = -0.33; P < 0.005) whereas delta5-DIOL, testosterone and SHBG were negatively correlated with apolipoprotein B levels (-0.32 < or = r < or = -0.43; P < 0.005). Statistical adjustment for visceral AT area, fasting insulin, fasting free fatty acid (FFA) levels and total body fat mass eliminated most of the correlations between steroid and lipoprotein levels, while SHBG remained significantly correlated with lipoprotein concentrations after such adjustments. Multivariate analyses revealed that SHBG, delta4-DIONE, delta5-DIOL and metabolic variables all contributed to the variance in plasma lipoprotein concentrations (from 10 to 29% of explained variance). Visceral AT, fasting FFA and insulin levels as well as SHBG concentrations appeared to be independent correlates of lipoprotein concentrations. Thus, metabolic and anthropometric variables examined in the present study could have represented important confounding factors in previous studies which have examined the relationship of steroid hormones to plasma lipoprotein concentrations.

Adipose Tissue↗

PubMed1997

Negative energy balance with exercise in identical twins: plasma glucose and insulin responses.

The effects of long-term (93 days) negative energy balance on plasma glucose and insulin were investigated by means of exercise with constant energy intake in seven pairs of young sedentary male identical twins. Results showed a significant decrease in fasting (-24%, P < 0.02) and postprandial insulin (-16%, P < 0.05). Fasting and postprandial plasma glucose and glucagon were not modified. Mean glucose disposal rate measured during a euglycemic-hyperinsulinemic clamp performed in five twin pairs was increased by 34% (P = 0.13). No significant intrapair similarity was found for the responses of fasting and postprandial insulin levels and of glucose disposal rate. Changes in glucose disposal rate were significantly greater in high compared with low losers for computerized tomography-measured abdominal visceral fat (3.0 +/- 1.1 vs. 0.3 +/- 0.5 mg x kg(-1) x min(-1), P < 0.05) despite similar losses in total body fat. We conclude that 1) a long-term negative energy balance generated by exercise training significantly reduces plasma insulin levels, whereas insulin sensitivity tends to be improved; 2) training-induced changes in insulin sensitivity are associated with changes in abdominal visceral fat; and 3) data from this experiment conducted with a small number of twin pairs suggest that the genotype does not seem to be a major determinant of the changes in insulin levels and sensitivity brought about by negative energy balance with exercise.

Abdomen↗

PubMed1997

Acute and chronic effects of exercise on leptin levels in humans.

The acute (single bout of exercise) and chronic (exercise training) effects of exercise on plasma leptin were investigated in 97 sedentary adult men (n = 51) and women (n = 46) participating in the HERITAGE Family Study. Exercise training consisted of a standardized 20-wk endurance training program performed in the laboratory on a computer-controlled cycle ergometer. Maximal oxygen uptake, body composition assessed by hydrostatic weighing, and fasting insulin level were also measured before and after training. Pre- and posttraining blood samples were obtained before and after completion of a maximal exercise test on the cycle ergometer. Exercise training resulted in significant changes in maximal oxygen uptake (increase in both genders) and body composition (reduction of fat mass in men and increase in fat-free mass in women). There were considerable interindividual differences in the leptin response to acute and chronic effects of exercise, some individuals showing either increase or reduction in leptin, others showing almost no change. On average, leptin levels were not acutely affected by exercise. After endurance training was completed, leptin levels decreased significantly in men (from 4.6 to 3.9 ng/ml; P = 0.004) but not in women. However, after the training-induced changes in body fat mass were accounted for, the effects of exercise training were no longer significant. Most of the variation observed in leptin levels after acute exercise or endurance training appears to be within the confidence intervals of the leptin assay. We conclude that there are no meaningful acute or chronic effects of exercise, independent of the amount of body fat, on leptin levels in humans.

Adolescent↗

PubMed1997

In situ hybridization analysis of ZPK gene expression during murine embryogenesis.

ZPK is a recently described protein serine/threonine kinase that has been originally identified from a human teratocarcinoma cell line by the polymerase chain reaction and whose function in signal transduction has not yet been elucidated. To investigate the potential role of this protein kinase in developmental processes, we have analyzed the spatial and temporal patterns of expression of the ZPK gene in mouse embryos of different gestational ages. Northern blot analysis revealed a single mRNA species of about 3.5 KB from Day 11 of gestation onwards. In situ hybridization studies demonstrated strong expression of ZPK mRNA in brain and in a variety of embryonic organs that rely on epitheliomesenchymal interactions for their development, including skin, intestine, pancreas, and kidney. In these tissues, the ZPK mRNA was localized primarily in areas composed of specific types of differentiating cells, and this expression appeared to be upregulated at a time concomitant with the onset of terminal differentiation. Taken together, these observations raise the possibility that the ZPK gene product is involved in the establishment and/or maintenance of a fully cytodifferentiated state in a variety of cell lineages.

Animals↗

PubMed1997

Androstane-3alpha,17beta-diol glucuronide as a steroid correlate of visceral obesity in men.

Plasma levels of androstane-3alpha,17beta-diol glucuronide (3alpha-DIOL-G) and androsterone glucuronide (ADT-G) as well as testosterone and adrenal C19 steroid concentrations were measured in a sample of 80 men in whom visceral adipose tissue (AT) accumulation was also determined by computed tomography. Plasma 3alpha-DIOL-G concentrations showed significant positive correlations with total body fat mass (r = 0.31; P < 0.05) and percent body fat (r = 0.28; P < 0.05). Furthermore, plasma 3alpha-DIOL-G levels were significantly associated with visceral adipose tissue accumulation (r = 0.41; P < 0.0005) as well as fasting plasma insulin (r = 0.35; P < 0.005) and glycemic and insulinemic responses to an oral glucose load (r = 0.39; P < 0.0005 and r = 0.32; P < 0.005, respectively). However, associations between 3alpha-DIOL-G and plasma glucose-insulin homeostasis indexes were no longer significant after adjustment for visceral AT area. ADT-G levels were not significantly associated with any of the adiposity variables. Subjects matched for abdominal sc AT area but with either low or high levels of visceral AT area showed significant differences in 3alpha-DIOL-G concentrations (P < 0.05), whereas subjects with low or high levels of abdominal sc AT but similar levels of visceral AT had similar 3alpha-DIOL-G concentrations. Among men with high testosterone levels, subjects with reduced 3alpha-DIOL-G concentrations had lower visceral adipose tissue accumulation than subjects with increased 3alpha-DIOL-G levels. The present results indicate that plasma 3alpha-DIOL-G, but not ADT-G, is a steroid correlate of visceral obesity. Excess visceral adipose tissue and/or concomitant alterations in insulin levels or in vivo insulin action could be responsible for the increased 3alpha-DIOL-G formation observed in this condition.

Adipose Tissue↗

PubMed1997

Hyperinsulinemia and abdominal obesity affect the expression of hypertriglyceridemia in heterozygous familial lipoprotein lipase deficiency.

We have reported three missense mutations (G188E, P207L, and D250N) in the lipoprotein lipase (LPL) gene among French-Canadians, resulting in the absence of measurable postheparin plasma LPL activity in homozygotes. Presence of triglyceride- and cholesterol-rich VLDL, as well as cholesterol-poor HDL particles, has been shown in heterozygotes affected by partial reduction in postheparin LPL activity. However, significant heterogeneity in their plasma triglyceride levels has been found, even among individuals carrying the same LPL gene mutation, indicating that factors other than LPL deficiency could affect the phenotypic expression of hypertriglyceridemia in the heterozygous state. The aim of the present study was to examine the combined effects of abdominal fat accumulation and hyperinsulinemia on plasma triglyceride levels among heterozygous patients for familial LPL deficiency. Based on sex and BMI, 43 heterozygotes (25 women and 18 men) were matched with noncarrier control subjects. Our data indicate that heterozygotes with higher abdominal fat deposition, as defined as waist girth values above the 50th percentile, had higher plasma triglyceride levels than nonobese heterozygotes. However, an important proportion of male heterozygote subjects were hypertriglyceridemic, even in absence of abdominal obesity, suggesting that another factor(s) was involved in the modulation of hypertriglyceridemia in these subjects. Indeed, multivariate analyses revealed that fasting hyperinsulinemia was a significant correlate of hypertriglyceridemia among these heterozygotes. Results of the present study indicate that abdominal obesity and hyperinsulinemia both have deleterious effects on plasma triglyceride levels in familial LPL deficiency. It is suggested that heterozygotes with moderate obesity and/or insulin resistance may be at higher risk of coronary artery disease because of the expression of an atherogenic lipoprotein phenotype among these patients.

Abdomen↗

PubMed1997

Linkage and association studies between the melanocortin receptors 4 and 5 genes and obesity-related phenotypes in the Québec Family Study.

BACKGROUND: The agouti yellow mouse shows adult onset of moderate obesity and diabetes. A depressed basal lipolytic rate in adipocytes or a decreased adrenergic tone arising from antagonizing alpha-melanocyte-stimulating hormone (MSH) activation of melanocortin receptors (MCR) could be at the origin of the obesity phenotype. MATERIAL AND METHODS: MCR 4 and 5 (MC4R, MC5R) genes were studied in the Québec Family Study. Sequence variations were detected by Southern blot probing of restricted genomic DNA, and mRNA tissue expression was detected by RT-PCR. Subjects with a wide range of weight were used for single-point sib-pair linkage studies (maximum of 289 sibships from 124 nuclear families). Analysis of variance across genotypes in unrelated males (n = 143) and females (n = 156) was also undertaken. Body mass index (BMI), sum of six skin-folds (SF6), fat mass (FM), percent body fat (%FAT), respiratory quotient (RQ), resting metabolic rate (RMR), fasting glucose and insulin, and glucose and insulin area during an oral glucose tolerance test were analyzed. RESULTS: MC4R showed polymorphism with NcoI, and MC5R, with PstI and PvuII, with a heterozygosity of 0.38, 0.10, and 0.20, respectively. Linkages were observed between MC5R and BMI (p = 0.001), SF6 (p = 0.005), FM (p = 0.001), and RMR (p = 0.002), whereas associations were observed in females between MC5R and BMI (p = 0.003), and between MC4R and FM (p = 0.002) and %FAT (p = 0.004). After correction for multiple tests, these p values are lowered by one tenth. MC4R and MC5R mRNAs have been detected in brain, adipose tissue, and skeletal muscle. CONCLUSIONS: MC4R and MC5R exhibit evidence of linkage or association with obesity phenotypes, but this evidence is strongest for MC5R.

Adolescent↗

PubMed1996

Familial correlations in the Québec family study: cross-trait familial resemblance for body fat with plasma glucose and insulin.

This study represents one component in our investigation of the familial factors underlying the insulin resistance (or metabolic) syndrome involving obesity, hyperinsulinaemia, glucose intolerance, dyslipidaemia, and hypertension. Here we examine the cross-trait familial resemblance between four measures of body size (two assessing total fat [body mass index and sum of six skinfolds] and two assessing fat patterning [ratio of trunk skinfold sum to extremity skinfold sum, adjusted and unadjusted for total subcutaneous fat]) with fasting plasma levels of glucose, insulin, and the ratio of insulin to glucose (IGR) in non-diabetic families participating in phase 1 of the Québec Family Study. A bivariate familial correlation model assessed both intraindividual (e.g. father's body size with father's insulin) and interindividual (e.g. father's body size with son's insulin) cross-trait associations. Intraindividual correlations suggested a greater degree of cross-trait associations for body fat (rather than fat distribution) measures with insulin and the IGR (rather than with glucose) levels. While the intraindividual correlations were significant for most cross-trait comparisons, only the sum of six skinfolds evidenced any familial association (i.e. interindividual resemblance) with insulin and the IGR. Specifically, cross-trait parent-offspring (but not sibling or spouse) correlations were significant, with a bivariate familiality estimate (i.e. polygenic and/or common familial environment) of about 8%. While the lack of sibling correlations does not suggest a simple familial hypothesis, a more complex genetic effect underlying the common covariation between total body fat with insulin and IGR cannot be ruled out.

Adolescent↗

PubMed1996

Role of body fat loss in the exercise-induced improvement of the plasma lipid profile in non-insulin-dependent diabetes mellitus.

The study was designed to examine the impact of exercise training on the plasma lipid profile in non-insulin-dependent diabetes mellitus (NIDDM) and, more particularly, to determine the relationship between changes in body fat mass and changes in the lipid profile. Eleven men with NIDDM exercised for 1 hour thrice per week on an ergocycle over a 6-month period at 60% maximal oxygen uptake (Vo2max). Diet and hypoglycemic agents were kept constant throughout this period. Vo2max, body composition, fasting plasma glucose and insulin levels, glycosylated hemoglobin, and the lipid profile were determined at baseline, in the middle (3 months), and at the end (6 months) of the training program. When the subjects were considered as a group, the only significant effect of training was on Vo2max, which increased from 32.2 +/- 1.2 mL/kg/min at baseline to 38.0 +/- 1.7 mL/kg/min at 6 months (P < .001). When the data were analyzed on an individual basis, significant associations were observed between changes in body fat mass and changes in the low-density lipoprotein (LDL) cholesterol/high-density lipoprotein (HDL) cholesterol ratio (r = .62,P = .04) or triglyceride (TG) levels (r = .64,P = .03). These data indicate that fat loss, not training per se, favorably alters the lipid profile of subjects with NIDDM who participate in an aerobic physical-conditioning program.

Adipose Tissue↗

PubMed1996

Effect of physical training on mitochondrial function in skeletal muscle of normal and diabetic rats.

The study was designed to assess the impact of physical training on the oxidative phosphorylation rate (OPR) in mitochondria isolated from two different skeletal muscles of rats with or without chronic diabetes mellitus. Diabetes was induced by an intravenous injection of streptozotocin (50 mg/kg), and only animals with a blood glucose level between 14 and 22 mmol/L 1 week later were kept in the protocol. Exercise training was performed on a treadmill with a progressive 10-week program. Rats were killed by decapitation at the end of the training program, and mitochondria were isolated from the gastrocnemius and the red vastus lateralis muscles. When the data were expressed as per milligrams of protein, OPR was significantly depressed by diabetes mellitus in the mitochondria from each muscle; a similar negative impact also appeared to be produced by physical training in mitochondria isolated from the red vastus lateralis muscle. However, due to changes in mitochondrial protein yield between groups, the capacity to oxidize pyruvate and malate was also calculated per gram of muscle. Adenosine triphosphate (ATP) production rate appeared to be unaffected by diabetes but significantly increased by training in both muscles of diabetic and nondiabetic rats. This effect of training was not associated with any improvement in plasma glucose or insulin levels in diabetic animals. However, the large increase in plasma levels of beta-hydroxybutyric acid in sedentary diabetic rats was partly reversed by training (1,079 +/- 472 v 3,424 +/- 618 micromol, P < .001). These results suggest that the training-induced increase in the capacity of skeletal muscles to oxidize substrates and generate energy may also contribute to reduce the elevated plasma beta-hydroxybutyric acid levels observed in a state of insulin deficiency. This may have clinical relevance, since ketoacidosis remains a life-threatening event in insulin-dependent diabetic subjects.

3-Hydroxybutyric Acid↗

PubMed1996

Plasma high-density lipoprotein cholesterol but not apolipoprotein A-I is a good correlate of the visceral obesity-insulin resistance dyslipidemic syndrome.

Apolipoprotein (apo) A-I is a major component of high-density lipoproteins (HDLs), and it has been suggested that measurement of apo A-I may provide additional information in the assessment of coronary heart disease (CHD) risk. In the present study in a sample of 111 men (age [mean +/- SD], 35.3 +/- 6.6 years), we determined whether a low apo A-I concentration is associated with the cluster of metabolic abnormalities that characterize the visceral obesity-insulin resistance dyslipidemic syndrome. For this purpose, the first and fourth quartiles of apo A-I and HDL cholesterol (HDL-C) concentrations were compared in relation to body fat distribution, glucose tolerance, and plasma insulin and lipoprotein levels. Men in the first quartile (< the 25th percentile) of HDL-C, as compared with men in the fourth quartile (> the 75th percentile), were characterized by an elevated visceral adipose tissue (AT) accumulation (P < .05), as well as by increased plasma levels of triglycerides ([TGs] P < .0001), apo B (P < .0005), and insulin (P < .01). These differences were not found when the first and fourth quartiles of plasma apo A-I concentrations were compared. These results suggest that plasma levels of HDL-C are more closely associated with the various features of the visceral obesity-insulin resistance syndrome than plasma apo A-I.

Adipose Tissue↗

PubMed1996

Overfeeding in identical twins: 5-year postoverfeeding results.

From a total of 12 pairs of young male identical twins who were overfed by an estimated 84,000 kcal over a period of 100 days, several pairs (eight to 11, depending on variables) were remeasured for body weight, body composition with the underwater weighing technique, regional fat distribution from skinfolds, girths, computed tomography (CT) fat areas in the abdominal region, and fasting plasma glucose, insulin, total cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides 4 months and 5 years after completion of the overfeeding protocol. At 4 months, the twins had lost approximately 7 of 8 kg that they had gained with overfeeding. However, 5 years later, body weight had increased by 5 kg over the preoverfeeding level. Fluctuations in fat mass were greater than those in fat-free mass. The younger twins gained approximately twice as much as the older twins in the late recovery period, a difference attributed to the late phase of growth in body mass in the former. Upper-body fat was reduced at 4 months of follow-up study, but was increased in the late recovery phase. All blood values were normalized in the postoverfeeding periods. A within-pair resemblance was generally observed for the changes noted in the recovery periods, but it was more striking when variations between preoverfeeding and 4-month or 5-year values were considered. We conclude from these observations that there were no persistent effects of exposure to the overfeeding protocol over the expected age-associated increases in body mass, body fat, upper-body fat, abdominal visceral fat (AVF), and metabolic variables predictive of risk for common diseases in individuals of normal body weight and with no family history of obesity. The intrapair resemblance suggests that the genotype contributes to the alterations observed in the recovery from overfeeding and in the age-associated changes.

Adipose Tissue↗

PubMed1996

Early insulin and glucagon responses to different food items.

An early postprandial insulin release has previously been described when high carbohydrate meals are fed. The present investigation on humans shows that this response takes place not only with high carbohydrate (sugar pie) but also with high lipid (whipped cream) and protein (beef steak or fish fillet) meals, suggesting that it is caused by the palatability of the food rather than to its composition. This increment takes place at the very beginning of the meal and even if the period of feeding lasted 10 min, the response has disappeared at that time. Thirty min later due to plasma glucose elevation, a significant increase in insulin was observed with the sugar pie. At that time a similar increase was observed with the fish filet or the beef steak but not with the whipped cream. A cephalic glucagon response was not observed with any of the meals but 30 min after feeding the plasma level of this hormone increased with both beef and fish feeding and decreased significantly with the sugar pie meal. The usefulness of these responses is discussed with relation to the metabolic responses associated with feeding.

Adult↗

PubMed1996

Postprandial glucose, insulin, and lipid responses to four meals containing unpurified dietary fiber in non-insulin-dependent diabetes mellitus (NIDDM), hypertriglyceridemic subjects.

OBJECTIVE: To evaluate the effects of two levels of total dietary fiber (10 g vs. 20 g) and two soluble:insoluble fiber ratios (1:4 vs. 2:3) on postprandial glucose and lipid metabolism in hypertriglyceridemic subjects with non-insulin-dependent diabetes mellitus (NIDDM). METHODS: Eight NIDDM, mildly hypertriglyceridemic subjects consumed four test breakfasts, each containing variable proportions of the same cereal and fruit fiber sources. Blood samples were obtained during the 4 hours following the test meals and analyzed for glucose, insulin, triglyceride, total cholesterol and high density lipoprotein cholesterol. RESULTS: The incremental area under the curve for glucose and insulin was lowered after consuming 20 g as compared to 10 g of dietary fiber (p < 0.05), but was not affected by the soluble insoluble fiber ratio. The postprandial lipemia was similar after all test meals. CONCLUSION: The proportion of soluble to insoluble fiber in cereal and fruit does not necessarily predict the effect of fiber on the glycemic response, while the overall quantity of fiber does appear to affect postprandial glucose metabolism in NIDDM.

Analysis of Variance↗