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Biomedical subjects

R N Bergman

Publications and source records attributed to R N Bergman.

At least 73 records · Page 4Linked to original sources
PubMed1996

Insulin sensitivity index, acute insulin response, and glucose effectiveness in a population-based sample of 380 young healthy Caucasians. Analysis of the impact of gender, body fat, physical fitness, and life-style factors.

BACKGROUND: Insulin sensitivity and insulin secretion are traits that are both genetically and environmentally determined. AIM: The aim of this study was to describe the distribution of the insulin sensitivity index (Si), the acute insulin response, and glucose effectiveness (Sg) in young healthy Caucasians and to estimate the relative impact of anthropometric and environmental determinants on these variables. METHODS: The material included 380 unrelated Caucasian subjects (18-32 yr) with measurement of Si, Sg and insulin secretion during a combined intravenous glucose (0.3 grams/kg body weight) and tolbutamide (3 mg/kg body weight) tolerance test. RESULTS: The distributions of Si and acute insulin response were skewed to the right, whereas the distribution of Sg was Gaussian distributed. Sg was 15% higher in women compared with men (P < 0.001). Waist circumference, body mass index, maximal aerobic capacity, and women's use of oral contraceptives were the most important determinants of Si. Approximately one-third of the variation of Si could be explained by these factors. Compared with individuals in the upper four-fifths of the distribution of Si, subjects with Si in the lowest fifth had higher waist circumference, higher blood pressure, lower VO2max, and lower glucose tolerance and fasting dyslipidemia and dysfibrinolysis. Only 10% of the variation in acute insulin response could be explained by measured determinants. CONCLUSION: Estimates of body fat, maximal aerobic capacity, and women's use of oral contraceptives explain about one-third of the variation in Si in a population-based sample of young healthy Caucasians.

Adolescent↗
PubMed1996

Causal linkage between insulin suppression of lipolysis and suppression of liver glucose output in dogs.

Suppression of hepatic glucose output (HGO) has been shown to be primarily mediated by peripheral rather than portal insulin concentrations; however, the mechanism by which peripheral insulin suppresses HGO has not yet been determined. Previous findings by our group indicated a strong correlation between free fatty acids (FFA) and HGO, suggesting that insulin suppression of HGO is mediated via suppression of lipolysis. To directly test the hypothesis that insulin suppression of HGO is causally linked to the suppression of adipose tissue lipolysis, we performed euglycemic-hyperinsulinemic glucose clamps in conscious dogs (n = 8) in which FFA were either allowed to fall or were prevented from falling with Liposyn plus heparin infusion (LI; 0.5 ml/min 20% Liposyn plus 25 U/min heparin with a 250 U prime). Endogenous insulin and glucagon were suppressed with somatostatin (1 microgram/min/kg), and insulin was infused at a rate of either 0.125 or 0.5 mU/min/kg. Two additional experiments were performed at the 0.5 mU/min/kg insulin dose: a double Liposyn infusion (2 x LI; 1.0 ml/min 20% Liposyn, heparin as above), and a glycerol infusion (19 mg/min). With the 0.125 mU/min/kg insulin infusion, FFA fell 40% and HGO fell 33%; preventing the fall in FFA with LI entirely prevented this decline in HGO. With 0.5 mU/min/kg insulin infusion, FFA levels fell 64% while HGO declined 62%. Preventing the fall in FFA at this higher insulin dose largely prevented the fall in HGO; however, steady state HGO still declined by 18%. Doubling the LI infusion did not further affect HGO, suggesting that the effect of FFA on HGO is saturable. Elevating plasma glycerol levels did not alter insulin's ability to suppress HGO. These data directly support the concept that insulin suppression of HGO is not direct, but rather is mediated via insulin suppression of adipose tissue lipolysis. Thus, resistance to insulin control of hepatic glucose production in obesity and/or non-insulin-dependent diabetes mellitus may reflect resistance of the adipocyte to insulin suppression of lipolysis.

Animals↗
PubMed1996

Transendothelial insulin transport is not saturable in vivo. No evidence for a receptor-mediated process.

In vitro, insulin transport across endothelial cells has been reported to be saturable, suggesting that the transport process is receptor mediated. In the present study, the transport of insulin across capillary endothelial cells was investigated in vivo. Euglycemic glucose clamps were performed in anesthetized dogs (n = 16) in which insulin was infused to achieve concentrations in the physiological range (1.0 mU/kg per min + 5 mU/kg priming bolus; n = 8) or pharmacologic range (18 mU/kg per min + 325 mU/kg priming bolus; n = 8). Insulin concentrations were measured in plasma and hindlimb lymph derived from interstitial fluid (ISF) surrounding muscle. Basal plasma insulin concentrations were twice the basal ISF insulin concentrations and were not different between the physiologic and pharmacologic infusion groups (plasma/ISF ratio 2.05 +/- 0.22 vs 2.05 +/- 0.23; p = 0.0003). The plasma/ISF gradient was, however, significantly reduced at steady-state pharmacologic insulin concentrations (1.37 +/- 0.25 vs 1.98 +/- 0.21; P = 0.0003). The reduced gradient is opposite to that expected if transendothelial insulin transport were saturable. Insulin transport into muscle ISF tended to increase with pharmacologic compared with physiologic changes in insulin concentration (41% increase; 1.37 +/- 0.18 10(-2) to 1.93 +/- 0.24 10(-2) min-1; P = 0.088), while at the same time insulin clearance out of the muscle ISF compartment was unaltered (2.53 +/- 0.26 10(-2) vs 2.34 +/- 0.28 10(-2) min-1; P = 0.62). Thus, the reduced plasma/ISF gradient at pharmacologic insulin was due to enhanced transendothelial insulin transport rather than changes in ISF insulin clearance. We conclude that insulin transport is not saturable in vivo and thus not receptor mediated. The increase in transport efficiency with saturating insulin is likely due to an increase in diffusionary capacity resulting from capillary dilation or recruitment.

Animals↗
PubMed1996

Extracellular glucose distribution is not altered by insulin: analysis of plasma and interstitial L-glucose kinetics.

We examined the effects of insulin on leg blood flow, whole body extracellular glucose distribution, and glucose diffusion into the interstitial fluid (ISF) surrounding skeletal muscle cells in anesthetized dogs. Extracellular glucose distribution and glucose diffusion into the muscle ISF were assessed by studying the kinetics of L-[1-14C]glucose in plasma and hindlimb lymph. Femoral artery blood flow was not increased with insulin (7.9 +/- 0.7 vs. 7.1 +/- 1.4 ml.min-1.kg-1; P = 0.54). Plasma and lymph dynamics of L-glucose after intravenous administration were superimposable between saline and insulin infusion experiments, indicating that insulin did not affect L-glucose disappearance from plasma or appearance in muscle ISF. Plasma L-glucose kinetics were best described by a four-compartment model, and one of the remote pools (intermediate) predicted the lymph L-glucose dynamics well. Estimation of maximum glucose diffusion capacity indicated that this pool, rather than the slowest pool, represents insulin-sensitive tissues. In conclusion, our data indicate that insulin does not increase transcapillary glucose diffusion to insulin-sensitive cells. In addition, hindlimb lymph represents primarily skeletal muscle ISF, which is represented by an intermediate, rather than the slowest, remote pool from whole body compartmental analysis.

3-O-Methylglucose↗
PubMed1996

Ethnic differences in carotid wall thickness. The Insulin Resistance Atherosclerosis Study.

BACKGROUND AND PURPOSE: Ethnic differences in cardiovascular disease (CVD) morbidity and mortality have been observed in US adults. However, little data exist on differences in indices of preclinical atherosclerosis such as carotid wall intima-media thickness (IMT) for US non-Hispanic whites, Hispanics, and blacks. This study was undertaken to determine whether there were ethnic differences in carotid wall IMT. METHODS: Internal carotid artery (ICA) IMT and common carotid artery (CCA) IMT, indices of atherosclerosis, were assessed with the use of B-mode ultrasound in 1020 nondiabetic participants in the Insulin Resistance Atherosclerosis Study, a multicenter study designed to examine the association between insulin resistance and carotid atherosclerosis. The study included 281 blacks, 329 Hispanics, and 410 non-Hispanic whites aged 40 to 69 years. RESULTS: Blacks had significantly greater CCA IMT than non-Hispanic whites (865 versus 808 microns); this remained significant after adjustment for major CVD risk factors and insulin sensitivity (864 versus 823 microns). There were no significant differences in ICA IMT between blacks and non-Hispanic whites. Hispanics had significantly lesser CCA IMT than non-Hispanic whites (749 versus 776 microns), and these differences remained significant after adjustment for traditional cardiovascular risk factors and insulin sensitivity (750 versus 778 microns). There were no significant differences in ICA IMT between non-Hispanic whites and Hispanics. CONCLUSIONS: We conclude that ethnic differences exist in CCA but not in ICA IMT in nondiabetic subjects. These differences in IMT, which are indicators of atherosclerosis, are a non-invasive measure that is consistent with some of the data on clinical end points. These differences may be associated with the observed differences in CVD morbidity and mortality among major ethnic groups in the United States.

Arteriosclerosis↗
PubMed1996

Toward an integrated phenotype in pre-NIDDM.

The search for the genetic basis of NIDDM has magnified the need for an efficient representation of the pre-NIDDM phenotype. The overall goal is to relate specific mutations on the genome to specific changes in physiologic function which lead to NIDDM. Unfortunately, there is still not a clear understanding of the molecular cause of NIDDM in most individuals. Therefore, one must take an alternative approach: to express in quantitative terms the various tissue processes which determine the ability to regulate the blood glucose in fasting and after carbohydrate administration. A minimal list of such processes includes the provision of glucose by the liver, insulin sensitivity, insulin secretion, and glucose effectiveness. The latter function is the ability of glucose per se to enhance glucose disappearance from blood, independent of a dynamic insulin response. Approaches to measuring the list of functions which determine the glucose tolerance are reviewed: they include the minimal model method, which quantitates insulin sensitivity (Sl) and glucose effectiveness (SG), and a combined model approach, which measures insulin secretion. These methods are being developed for large populations. Such a development is important for elucidating the causes of reduced glucose tolerance in populations, and examining the relation between such causes and outcomes including diabetes and cardiovascular disease. Of particular importance for diabetes development is the characteristic hyperbolic relationship between insulin secretion and insulin action. This relationship, the "hyperbolic law of glucose tolerance' indicates that insulin secretion can only be assessed in terms of the ambient degree of insulin sensitivity. By applying this principle, it is clear that latent pancreatic islet-cell dysfunction has been underestimated, and may be significant even in subjects with impaired glucose tolerance. Finally, new explorations of insulin control of liver glucose output indicate that this process may be under the control of free fatty acids. The latter realization indicates that the insulin effect on lipolysis is what is critical for determination of glucose output in the fasting state, and that insulin resistance at the level of the adipocyte may determine the extent of fasting hyperglycaemia, and may be an important factor in the overall phenotype in prediabetic and NIDDM individuals.

Animals↗
PubMed1995

OOPSEG: a data smoothing program for quantitation and isolation of random measurement error.

We describe a data smoothing program, OOPSEG, which automatically quantitates and filters the random measurement error in a given data series. The measurement error is initially guessed, and the Optimal Segments technique is used to filter a corresponding amount of variation from the data, thus generating a relatively smooth curve. The residuals about this smooth curve are tested for serial correlation. If correlation is detected, a new measurement error is guessed, and the data are filtered again. This process continues until a smooth curve has been found for which the residuals do not exhibit serial correlation. Such residuals represent the random component of the data, i.e. (presumably) the measurement error. The corresponding smooth curve thus approximates the original, error-free curve. The smooth curve and the estimated coefficient of variation of the data are returned. OOPSEG handles end effects by performing an expansion of the data set, smoothing this expanded data set, then deleting the artificial points before assembling the final, smooth curve. Also, data may be smoothed as a sequence of independent regions to accommodate time courses with known changes in experimental conditions. We suggest that OOPSEG may have numerous applications in data analysis and experimental design.

Algorithms↗
PubMed1995

Estimation of TCA cycle flux, aminotransferase flux, and anaplerosis in heart: validation with syntactic model.

Weiss et al. (Circ. Res. 70: 392-408, 1992) proposed a model of the citric acid cycle (CAC) in myocytes and a system of 17 differential equations that can be used to describe the changes over time in enrichment of carbons C-2 and C-4 of glutamate under conditions of metabolic steady state. They also proposed an empirical measure (KT) of flux through the CAC, which has been shown to be correlated to O2 consumption in rat hearts perfused with acetate or a mixture of glucose and acetate. We report a new method for estimation of the absolute rate of the flux through the CAC in heart (vTCA), without the numerical solution of differential equations. Unlike KT, our estimate is equal to the rate of flux catalyzed by the alpha-ketoglutarate dehydrogenase complex (vTCA), not merely correlated with it. We also estimate the rate of flux catalyzed by aspartate aminotransferase (vTA) and by NADP(+)-dependent malic enzyme (an anaplerotic reaction). The formula for vTCA during administration of [2-13C]acetate is as follows: vTCA = M[(C-2ssLC-4)/[C-4ss(LC-4-LC-2)]], where C-2ss and C-4ss represent steady-state fractional enrichment, LC-2 and LC-4 represent dominant rate constants of C-2 and C-4 of glutamate, respectively, and M is the sum of concentrations of aspartate, glutamate, and intermediates of the CAC. The assumptions underlying our formula are as follows: 1) metabolic steady state is maintained, 2) exchange of molecules between cytosolic and mitochondrial compartments is rapid, 3) 13C enters pools of the CAC only from acetyl CoA via citrate synthase, 4) [citrate]/[glutamate] < 1 + (vTCA/vTA), and 5) (m-[glutamate])/M < C-2ss/C-4ss.

Aspartate Aminotransferases↗
PubMed1995

Insulin sensitivity accounts for glucose and lactate kinetics after intravenous glucose injection.

Mathematical modeling was used to explore the interaction between glucose, insulin, and lactate during the frequently sampled intravenous glucose tolerance test (FSIGTT). Insulin-modified FSIGTs were performed in 25 lean volunteers, and an additional 5 volunteers underwent FSIGTs with glucose injection alone to illustrate the effect of insulin on both glucose and lactate kinetics. The model chosen as the best representation of the system extended the minimal model of glucose kinetics (MM) by including a two-compartment model of lactate kinetics. The model accounted for both glucose and lactate kinetics, provided traditional MM parameters of insulin sensitivity and glucose effectiveness, and descriptive parameters of lactate kinetics. Modeling suggested that lactate production was limited by the rate of glucose disappearance, with no indication of direct effects of insulin on lactate. Inclusion of lactate kinetics had no adverse effect on MM parameters (SG: 0.023 +/- 0.009 vs. 0.023 +/- 0.010 min-1, SI: 1.01 +/- 0.70 vs. 1.03 +/- 0.71 x 10(4).min-1.pmol-1.1; P > 0.50, lactate model vs. MM), and indicated that approximately 1.2% min-1 of total glucose disappearance during the FSIGT is converted to lactate. An additional benefit of including lactate kinetics was the significant improvement in precision in MM parameter estimates as reflected by the fractional standard deviations (FSDs). This effect was most prominent for SG, in which a threefold improvement in parameter precision was observed (FSD: 13.5 +/- 3.1 vs. 42.5 +/- 48.5; means +/- SD).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Free fatty acid as a link in the regulation of hepatic glucose output by peripheral insulin.

Overproduction of glucose by the liver in the face of insulin resistance is a primary cause of hyperglycemia in non-insulin-dependent diabetes mellitus (NIDDM). However, mechanisms involved in control of hepatic glucose output (HGO) remain less than clear, even in normal individuals. Recent results have supported an indirect extrahepatic effect of insulin as the primary locus of insulin action to restrain HGO. One suggested extrahepatic site is the pancreatic alpha-cell. To examine whether insulin's extrahepatic site is independent of the alpha-cells, HGO suppression was examined independent of changes in glucagon secretion or insulin antagonism of glucagon action. Euglycemic glucose clamps (n = 40) with somatostatin infusion were performed in conscious dogs (n = 5). Paired experiments were conducted in which insulin was infused either portally (1.2, 3.0, 6.0 pmol.min-1.kg-1) or peripherally at half the portal infusion rate (0.6, 1.5, 3.0 pmol.min-1.kg-1). Additional zero and saturating portal-dose experiments (100 pmol.min-1.kg-1) were also performed. For the paired experiments, portal insulin infusion resulted in portal insulin concentrations approximately two to three times higher than in the corresponding peripheral insulin infusion experiments, while at the same time peripheral insulin concentrations were approximately matched. Equal peripheral insulin concentration resulted in equivalent HGO suppression irrespective of the portal concentrations. Thus, insulin affects a signal at a peripheral site, other than alpha-cell, that in turn suppresses hepatic glucose production. To investigate the nature of this signal, we measured alanine, lactate, and free fatty acids (FFAs).(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine↗
PubMed1995

Studies of reproductive competence in male Dirofilaria immitis treated with milbemycin oxime.

Normal adult Dirofilaria immitis from a microfilaremic donor dog and D. immitis from donors rendered microfilaria (MF) negative by seven consecutive monthly doses of milbemycin oxime (500 micrograms/kg) were transplanted into three previously uninfected and untreated dogs. Two dogs received reciprocal combinations of treated and untreated D. immitis and the third received untreated adults of both sexes. A fourth dog served as an infected, milbemycin treated, non-transplanted control. Eleven weeks after pairing treated female with untreated male worms, a low-level microfilaremia developed in the recipient. Two of the three treated female worms recovered from this dog were non-fertile, and the third contained a small number of elongate and coiled embryos but no mature intrauterine (stretched) microfilariae (MFF). The dog receiving treated male and untreated female worms became microfilaremic after two weeks. Microfilaremia peaked at 37,000/ml 16 weeks after transplantation and declined over the next 20 weeks to 7,200/ml. Untreated females paired with treated males either became non-fertile or exhibited low numbers of developing embryos and MFF scattered throughout their reproductive tracts. Pairing of untreated male and female worms produced a mcirofilaremia during the second post-operative week, which plateaued around 15,000 MFF per ml. Females recovered after this pairing contained a normal pattern of embryonic development, including stretched MFF. There were no significant differences in the percentage composition or absolute numbers of developing and mature sperm in the reproductive tracts of treated and untreated male worms. However, the resumption of MF production in one milbemycin treated female worm after pairing with normal males and failure of treated males to sustain MF production in untreated female worms suggest that milbemycin oxime impairs the sexual competence of male D. immitis. This may explain the ability of this drug to bring about long term suppression of microfilaremia without immediate adulticidal activity.

Animals↗
PubMed1994

Primacy of liver glucosensors in the sympathetic response to progressive hypoglycemia.

The impact of hepatic glucose concentration on the sympathetic response to progressive hypoglycemia was examined in chronically cannulated conscious male dogs (n = 6). Graded hypoglycemia was induced via peripheral insulin infusion (30 pmol.kg-1.min-1) with either peripheral (PER) or portal (POR) glucose infusion. Over the 260-min experimental period, arterial glycemia was adjusted from 5.2 +/- 0.1 to 2.5 +/- 0.1 mM in decrements of approximately 0.5 mM every 40 min. Arterial glycemias were not significantly different between PER and POR at any measured level. However, hepatic glycemia was significantly elevated at all times during POR (8.4 +/- 0.8 to 3.4 +/- 0.2 mM) when compared to PER (5.2 +/- 0.2 to 2.5 +/- 0.1 mM). Plasma epinephrine values were significantly greater during PER vs. POR at all arterial glycemias below 4.0 mM. At the lowest level of arterial glycemia studied (2.5 +/- 0.2 mM) the epinephrine response above basal was 3-fold greater for PER (8.7 +/- 1.7 nM) when compared to POR (2.6 +/- 0.6 nM) (P < 0.01). Plasma norepinephrine results were similar for the two protocols, with PER demonstrating a 3-fold greater response above basal when compared to POR at 2.5 mM arterial glycemia (P < 0.05). While the sympathetic response was markedly different between protocols when expressed as a function of arterial glycemia, when expressed as a function of hepatic glycemia this discrepancy was largely eliminated. This latter observation supports the liver as the primary locus for glycemic detection relevant to the sympathoadrenal response when hypoglycemia develops slowly--i.e., over a period of 2-3 h. A comparison of the current findings with our previous observations suggests that the hepatic glucosensors may play a greater role in hypoglycemic counterregulation as the rate of fall in glycemia is less.

Animals↗
PubMed1994

SYNTAX: a rule-based stochastic simulation of the time-varying concentrations of positional isotopomers of metabolic intermediates.

We present a new approach to simulation of metabolic pathways. The syntactic approach combines a rule-based description of biochemical reactions with a stochastic model of chemical kinetics. Each syntactic rule describes the location in a product molecule to which a particular carbon of a reactant molecule will be transferred. Using specifically labeled substrates and known rates of chemical reactions, our simulation predicts the time-dependent changes in concentration of positional isotopomers of metabolic intermediates. (A positional isotopomer of a compound is an isomer that is determined by the positions of isotopes within the molecule, e.g., [1,2-13C]glucose and [1,3,5-13C]glucose). For the simulation of the 13C-positional isotopomers of the citric acid cycle in heart cells we require only 39 syntactic rules, compared to the 176 ordinary differential equations required by the traditional approach. Addition of chemical reactions to the simulation does not require changing the program code for the existing reactions. In comparison, addition of a reaction to a system described by differential equations requires altering the equations for all isotopomers of all reactants and products of the new chemical reaction.

Carbon Isotopes↗
PubMed1994

Importance of transcapillary insulin transport to dynamics of insulin action after intravenous glucose.

Insulin action in vivo is determined by both transendothelial insulin transport (TET) across the capillary and subsequent insulin binding and postreceptor events. To examine TET under non-steady-state conditions, we performed intravenous glucose tolerance tests (IVGTT; 0.3 g/kg; n = 7) on conscious dogs. At basal, insulin in lymph was only 53 +/- 7% of plasma insulin (P < 0.001), whereas lymph glucose exceeded plasma levels (109 +/- 4 vs. 104 +/- 4 mg/dl, respectively; P < 0.02). On injection, dynamics of glucose in plasma and lymph were similar, suggesting rapid equilibration of glucose between compartments. In contrast, insulin appearance in lymph was delayed relative to plasma (5.1 +/- 1.3 vs. 2 +/- 0 min), peaked later (21 +/- 2 vs. 8 +/- 2 min), attained peak value of only 52 +/- 6% of plasma insulin (range, 35-76%), and remained lower than plasma insulin throughout the IVGTT (P < 0.05 or better). Minimal model-derived insulin sensitivity (SI) averaged 3.55 +/- 0.75 x 10(-4) min-1/(microU/ml). There was a strong linear relationship between lymph insulin and its effect on glucose disappearance [X(t), r = 0.95 +/- 0.01]. Determination of the relative contributions of TET and post-TET insulin-sensitive processes to overall SI revealed that cellular sensitivity to interstitial insulin dominated (r2 = 0.55), but was not the exclusive determinant of, overall SI, as insulin transport was also important (r2 = 0.21). TET is a previously unrecognized contributor to SI in vivo.

Animals↗
PubMed1994

Prediction of positional isotopomers of the citric acid cycle: the syntactic approach.

We propose a syntactic approach to modeling of biochemical fluxes that combines a rule-based description of atomic transfer in chemical reactions with a structurally oriented, stochastic model of chemical reaction kinetics. This approach avoids the use of differential equations to describe the production and disappearance of each molecule. The computer simulation predicts the changes over time in the abundance of each positional isotopomer of every metabolic intermediate in the citric acid cycle of heart cells, subsequent to administration of [2-13C]acetate (including natural abundance of 13C). (Positional isotopomers are isomers that differ in the positions of isotopes within the molecule.) The 32 positional isotopomers of glutamate fell into four groups with similar intragroup dynamics but with very different amplitudes. From the relative abundance of each isotopomer of glutamate, we calculate the relative area of multiplets of the nuclear magnetic resonance spectrum.

Acetates↗
PubMed1994

Dietary restriction increases insulin sensitivity and lowers blood glucose in rhesus monkeys.

Insulin sensitivity and glucose tolerance typically decline during later life. In a multidimensional randomized trial of the effects of dietary restriction started in adulthood on the processes of aging, we are studying insulin sensitivity and glucoregulation longitudinally in control (C, n = 15, fed a defined diet ad libitum for 6-8 h/day) and restricted (R, n = 15, fed 30% less than C) monkeys using the Modified Minimal Model method. Linear rates of change were calculated for individual animals through 30 mo of diet treatment and compared between treatment groups. Basal glucose, basal insulin, and insulin responses to glucose and tolbutamide increased for C and decreased for R animals (P < or = 0.002), whereas insulin sensitivity decreased for C and increased for R (P = 0.008). Glycosylated hemoglobin at 30 mo was marginally lower in R (P = 0.06) and was positively correlated with fasting plasma glucose (r = 0.508, P < 0.001). Insulin changes were significantly correlated with changes in adiposity (weight and abdominal circumference). Identification of the mechanisms through which these effects are achieved may aid in ameliorating glucose intolerance, insulin resistance, and associated illnesses in older persons.

Animals↗