Biomedical subjects

Joseph A Houmard

Publications and source records attributed to Joseph A Houmard.

At least 19 recordsLinked to original sources

PubMed2007

Modest exercise prevents the progressive disease associated with physical inactivity.

Activity levels continue to decline as technology continues to engineer movement out of our environment. We summarize the findings from Studies Targeting Risk Reduction Interventions through Defined Exercise (STRRIDE) emphasizing the high cost of even short-term continued inactivity in sedentary, overweight, or mildly obese individuals. There seems to be a critical minimal level of physical activity required to maintain metabolic health. A modest amount of exercise seems to prevent metabolic deterioration.

Cardiovascular Diseases↗

PubMed2006

Expression of genes regulating malonyl-CoA in human skeletal muscle.

In humans and animal models, increased intramuscular lipid (IML) stores have been implicated in insulin resistance. Malonyl-CoA plays a critical role in cellular lipid metabolism both by serving as a precursor in the synthesis of lipids and by inhibiting lipid oxidation. In muscle, Malonyl-CoA acts primarily as a negative allosteric regulator of carnitine palmitoyl transferase-1 (CPT1) activity, thereby blocking the transport of long chain fatty acyl CoAs into the mitochondria for oxidation. In muscle, increased malonyl-CoA, decreased muscle CPT1 activity, and increased IML have all been reported in obesity. In order to determine whether malonyl-CoA synthesis might be under transcriptional as well as biochemical regulation, we measured mRNA content of several key genes that contribute to the cellular metabolism of malonyl-CoA in muscle biopsies from lean to morbidly obese subjects. Employing quantitative real-time PCR, we determined that expression of mitochondrial acetyl-CoA carboxylase 2 (ACC2) was increased by 50% with obesity (P < 0.05). In both lean and obese subjects, expression of mitochondrial ACC2 was 20-fold greater than that of cytoplasmic ACC1, consistent with their hypothesized roles in synthesizing malonyl-CoA from acetyl-CoA for CPT1 regulation and lipogenesis, respectively. In addition, in both lean and obese subjects, expression of malonyl-CoA decarboxylase was approximately 40-fold greater than fatty acid synthase, consistent with degradation, rather than lipogenesis, being the primary fate of malonyl-CoA in human muscle. No other genes showed signs of increased mRNA content with obesity, suggesting that there may be selective transcriptional regulation of malonyl-CoA metabolism in human obesity.

Acetyl-CoA Carboxylase↗

PubMed2006

GRB14, GPD1, and GDF8 as potential network collaborators in weight loss-induced improvements in insulin action in human skeletal muscle.

Obesity is associated with insulin resistance in skeletal muscle; accordingly, weight loss dramatically improves insulin action. We sought to identify molecular remodeling of muscle commensurate with weight loss that could explain improvements in insulin action. Muscle from morbidly obese women was studied before and after gastric bypass surgery. Gastric bypass surgery significantly reduced body mass by approximately 45% and improved insulin action. We then assessed mRNA profiles using a stringent statistical analysis (statistical concordance with three probe set algorithms), with validation in a cross-sectional study of lean (n = 8) vs. morbidly obese (n = 8) muscle. Growth factor receptor-bound protein 14 (GRB14), glycerol-3-phosphate dehydrogenase 1 (GPD1), and growth differentiation factor 8 (GDF8; myostatin) significantly decreased approximately 2.4-, 2.2-, and 2.4-fold, respectively, after weight loss (gastric bypass). Increased expression of these transcripts was associated with increased obesity in the cross-sectional group (lean vs. morbidly obese muscle). Each transcript was validated by real-time quantitative RT-PCR assays in both study groups. Using Ingenuity Pathway Analysis, we show that all three transcripts are involved in the same regulatory network including AKT1, IGF1, TNF, PPARG, and INS. These results suggest that GRB14, GPD1, and GDF8 are weight loss-responsive genes in skeletal muscle and that the observed transcriptional modulation of these would be expected to improve insulin signaling, decrease triglyceride synthesis, and increase muscle mass, respectively, with weight loss. Thus our data provide a possible regulatory pathway involved in the development of insulin resistance in the morbidly obese state, and improvement of insulin resistance with weight loss.

Adaptor Proteins, Signal Transducing↗

PubMed2006

Response of high-sensitivity C-reactive protein to exercise training in an at-risk population.

BACKGROUND: High-sensitivity C-reactive protein (hsCRP) is promoted as an independent predictor of atherosclerotic risk. In addition, cardiorespiratory fitness is inversely related to hsCRP in single-sex cross-sectional analyses. Our objective was to determine if modulating fitness with exercise training imposes changes in high-sensitivity C-reactive protein in a mixed-sex population at risk for cardiovascular disease. METHODS: We studied baseline and postintervention plasma hsCRP in 193 sedentary, overweight to mildly obese, dyslipidemic men and women who were randomized to 6 months of inactivity or 1 of 3 aerobic exercise groups: low amount-moderate intensity (energy equivalent of approximately 19.3 km/wk at 40%-55% peak VO2), low amount-high intensity (energy equivalent of approximately 19.3 km/wk at 65%-80% peak VO2), or high amount-high intensity (energy equivalent of approximately 32.2 km/wk at 65%-80% peak VO2). RESULTS: At baseline, the study population was at intermediate to high cardiovascular risk as defined by hsCRP. Cardiorespiratory fitness was inversely related to hsCRP (P < .001) even after adjusting for significant and expected sex differences. Fitness, hormone replacement therapy use, and high-density lipoprotein cholesterol accounted for the sex difference in baseline hsCRP. Fitness, high-density lipoprotein cholesterol, fasting insulin, hormone replacement therapy, and visceral adiposity were all independent predictors for baseline hsCRP (r2 = 0.34 for the entire model, P < .0001). However, despite significant improvements in fitness, visceral adiposity, subcutaneous adiposity, and insulin sensitivity, hsCRP did not change in response to exercise training (P > .20). CONCLUSIONS: Cardiorespiratory fitness is inversely related to hsCRP independent of sex and accounts for most of the large sex disparity in hsCRP. Nonetheless, in the absence of a significant change in diet, 6 months of aerobic exercise training does not produce a significant change in hsCRP in an at-risk population.

Adult↗

PubMed2006

Skeletal muscle fat oxidation is increased in African-American and white women after 10 days of endurance exercise training.

OBJECTIVE: Obesity is associated with lower rates of skeletal muscle fatty acid oxidation (FAO), which is linked to insulin resistance. FAO is reduced further in obese African-American (AAW) vs. white women (CW) and may also be lower in lean AAW vs. CW. In lean CW, endurance exercise training (EET) elevates the oxidative capacity of skeletal muscle. Therefore, we determined whether EET would elevate skeletal muscle FAO similarly in AAW and CW with a lower lipid oxidative capacity. RESEARCH METHODS AND PROCEDURES: In vitro rates of FAO were assessed in rectus abdominus muscle strips using [1- 14C] palmitate (Pal) from lean AAW [BMI = 24.2 +/- 0.9 (standard error) kg/m2] and CW (23.6 +/- 0.8 kg/m2) undergoing voluntary abdominal surgery. Lean AAW (22 +/- 0.9 kg/m(2)) and CW (24 +/- 0.8 kg/m2) and obese AAW (36 +/- 1.2 kg/m2) and CW (40 +/- 1.3 kg/m2) underwent 10 consecutive days of EET on a cycle ergometer (60 min/d, 75% peak oxygen uptake). FAO was measured in vastus lateralis homogenates as captured 14CO2 using [1- 14C] Pal, palmitoyl-CoA (Pal-CoA), and palmityl-carnitine (Pal-Car). RESULTS: Muscle strip experiments showed suppressed rates of FAO (p = 0.03) in lean AAW vs. CW. EET increased the rates of skeletal muscle Pal oxidation (p = 0.05) in both lean AAW and CW. In obese subjects, Pre-EET Pal (but not Pal-CoA or Pal-Car) oxidation was lower (p = 0.05) in AAW vs. CW. EET increased Pal oxidation 100% in obese AAW (p < 0.05) and 59% (p < 0.05) in obese CW. Similar increases (p < 0.05) in post-EET FAO were observed for Pal-CoA and Pal-Car in both groups. DISCUSSION: Both lean and obese AAW possess a lower capacity for skeletal muscle FAO, but EET increases FAO similarly in both AAW and CW. These data suggest the use of EET for treatment against obesity and diabetes for both AAW and CW.

Adult↗

PubMed2006

Glucose transporter expression in skeletal muscle of endurance-trained individuals.

UNLABELLED: Two recently identified glucose transporters, GLUT8 and GLUT12, are expressed in human skeletal muscle and may be involved in insulin-mediated sugar transport. PURPOSE: The purpose of this study was to measure GLUT8 and GLUT12 mRNA levels in endurance-trained versus sedentary individuals in an effort to determine the effect of repeated days of contractile activity on gene expression. METHODS: GLUT 4, 8, and 12 mRNA were measured in biopsies from the vastus lateralis using quantitative real-time PCR in endurance-trained (N=16, age=22.0+/-0.9 yr, VO(2 max) (L.min(-1))=4.13+/-0.25) and sedentary (N=15, age=21.3+/-0.8 yr, VO(2 max) (L.min(-1))=3.21+/-0.24) subjects. RESULTS: GLUT12 mRNA was lower (40+/-14%, P<0.05) in the exercise-trained compared with the sedentary subjects. There was no difference between groups in GLUT8 mRNA content. mRNA of the insulin-sensitive glucose transporter (GLUT4) was 78+/-27% (P<0.05) higher in skeletal muscle from endurance-trained compared with sedentary individuals. CONCLUSION: These findings suggest an isoform-specific effect on the mRNA of the glucose transporters in human skeletal muscle with repeated days of contractile activity.

Adult↗

PubMed2005

Inactivity, exercise, and visceral fat. STRRIDE: a randomized, controlled study of exercise intensity and amount.

Despite the importance of randomized, dose-response studies for proper evaluation of effective clinical interventions, there have been no dose-response studies on the effects of exercise amount on abdominal obesity, a major risk factor for metabolic syndrome, diabetes, and cardiovascular disease. One hundred seventy-five sedentary, overweight men and women with mild to moderate dyslipidemia were randomly assigned to participate for 6 mo in a control group or for approximately 8 mo in one of three exercise groups: 1) low amount, moderate intensity, equivalent to walking 12 miles/wk (19.2 km) at 40-55% of peak oxygen consumption; 2) low amount, vigorous intensity, equivalent to jogging 12 miles/wk at 65-80% of peak oxygen consumption; or 3) high amount, vigorous intensity, equivalent to jogging 20 miles/wk (32.0 km). Computed tomography scans were analyzed for abdominal fat. Controls gained visceral fat (8.6 +/- 17.2%; P = 0.001). The equivalent of 11 miles of exercise per week, at either intensity, prevented significant accumulation of visceral fat. The highest amount of exercise resulted in decreased visceral (-6.9 +/- 20.8%; P = 0.038) and subcutaneous (-7.0 +/- 10.8%; P < 0.001) abdominal fat. Significant gains in visceral fat over only 6 mo emphasize the high cost of continued inactivity. A modest exercise program, consistent with recommendations from the Centers for Disease Control/American College of Sports Medicine (CDC/ACSM), prevented significant increases in visceral fat. Importantly, a modest increase over the CDC/ACSM exercise recommendations resulted in significant decreases in visceral, subcutaneous, and total abdominal fat without changes in caloric intake.

Abdominal Fat↗

PubMed2005

Elevated stearoyl-CoA desaturase-1 expression in skeletal muscle contributes to abnormal fatty acid partitioning in obese humans.

Obesity and type 2 diabetes are strongly associated with abnormal lipid metabolism and accumulation of intramyocellular triacylglycerol, but the underlying cause of these perturbations are yet unknown. Herein, we show that the lipogenic gene, stearoyl-CoA desaturase 1 (SCD1), is robustly up-regulated in skeletal muscle from extremely obese humans. High expression and activity of SCD1, an enzyme that catalyzes the synthesis of monounsaturated fatty acids, corresponded with low rates of fatty acid oxidation, increased triacylglycerol synthesis and increased monounsaturation of muscle lipids. Elevated SCD1 expression and abnormal lipid partitioning were retained in primary skeletal myocytes derived from obese compared to lean donors, implying that these traits might be driven by epigenetic and/or heritable mechanisms. Overexpression of human SCD1 in myotubes from lean subjects was sufficient to mimic the obese phenotype. These results suggest that elevated expression of SCD1 in skeletal muscle contributes to abnormal lipid metabolism and progression of obesity.

Body Mass Index↗

PubMed2005

Analysis of insulin-stimulated insulin receptor activation and glucose transport in cultured skeletal muscle cells from obese subjects.

Obesity is associated with impaired insulin-stimulated glucose disposal in the skeletal muscle, but whether this is an intrinsic or acquired factor is unknown. In many patients with type 2 diabetes mellitus (T2D) and their nondiabetic relatives, who have a genetic predisposition for diabetes, insulin resistance is maintained in cultured muscle cells. To study the association of obesity with defects in insulin action, we investigated insulin stimulation of both insulin receptor (IR) autophosphorylation and subsequent glucose transport in primary skeletal muscle cell cultures obtained from both nonobese and obese nondiabetic subjects. In these 2 groups, there was no difference in the ability of insulin to induce autophosphorylation of the IR, phosphorylation of the downstream serine kinase Akt/PKB, or stimulation of glucose transport. Moreover, there were no major differences in cultured muscle cell content of either the IR, the IR antagonist PC-1, or GLUT 1 and GLUT 4. These data therefore indicate that the insulin resistance associated with obesity is not maintained in cultured muscle cells and suggest that this insulin resistance is an acquired feature of obesity.

Adult↗

PubMed2005

Fat as an endocrine organ: influence of exercise.

The prevalence of diabetes and obesity continues to increase. It is therefore important to identify the pathophysiology underlying these disorders. An inability of insulin to stimulate glucose uptake, i.e., insulin resistance, appears to be a common link between diabetes and obesity. The identification of various adipocyte-secreted cytokines (adipocytokines) that influence satiety, energy balance, and insulin sensitivity provide a novel target for the treatment of these disorders. Adipocytokines are differentially expressed with obesity and diabetes, making them a strong candidate for linking insulin resistance to these pathological conditions. This review explores the role of adipocytokines in insulin action and examines the effect of exercise training on adipocytokine content.

Adipose Tissue↗

PubMed2005

Glucose uptake in muscle cell cultures from endurance-trained men.

PURPOSE: To examine noninsulin- (basal) and insulin-mediated glucose uptake in human skeletal muscle cells from endurance-trained and sedentary individuals. METHODS: Muscle biopsies (vastus lateralis) were obtained from competitive, endurance-trained athletes (N=12; VO2peak 64.9+/-2.3 mL.kg-1.min-1) and their sedentary counterparts (N=8; VO2peak 51.8+/-2.2 mL.kg-1.min-1), and isolated satellite cells allowed to proceed to myotubes. RESULTS: The myotubes exhibited a dose response for glucose uptake with increasing insulin concentrations; maximal glucose uptake was approximately 1.5-fold over basal. In relation to exercise training status, basal glucose uptake was significantly (P<0.05) elevated by approximately 75% in the endurance-trained versus sedentary men (20.1+/-2.1 vs 11.9+/-1.9 pmol.mg protein-1.min-1, respectively). This difference persisted at insulin concentrations of 10 and 1000 etaM, although the relative increase in insulin-mediated glucose uptake (fold increase over basal) did not differ between the sedentary and endurance-trained cells. CONCLUSIONS: These data suggest that cultured skeletal muscle cells from endurance-trained athletes may differ in respect to basal glucose uptake.

Adult↗

PubMed2005

Effects of exercise training amount and intensity on peak oxygen consumption in middle-age men and women at risk for cardiovascular disease.

STUDY OBJECTIVES: Although increasing aerobic fitness by exercise training is advocated as part of a healthy lifestyle, studies examining the different effects of intensity and amount on peak consumption (V(O2)) remain sparse. DESIGN: This randomized controlled trial compared the effects of three different exercise regimens differing in amount and intensity on fitness improvements. PARTICIPANTS: Overweight men and women with mild-to-moderate dyslipidemia were recruited. INTERVENTIONS: The exercise groups were as follows: (1) low amount/ moderate intensity (LAMI, n = 25), the caloric equivalent of walking 19 kilometers (km)/wk at 40 to 55% of peak V(O2); (2) low amount/high intensity (LAHI, n = 36), the equivalent of jogging 19 km/wk at 65 to 80% of peak V(O2); (3) high amount/high intensity (HAHI, n = 35), the equivalent of jogging 32 km/wk at 65 to 80% of peak V(O2); and (4) a control group (n = 37). MEASUREMENTS AND RESULTS: Peak V(O2) and time to exhaustion (TTE) were tested before and after 7 to 9 months of training. All exercise groups increased peak V(O2) and TTE compared to baseline (p < or = 0.001). Improvements in peak V(O2) were greater in the LAHI and HAHI groups compared to the control group (p < 0.02); HAHI group improvements were greater than the LAMI group (p < 0.02) and the LAHI group (p < 0.02). Increased TTE for all exercise groups was higher compared to the control group (p < 0.001) CONCLUSIONS: Exercising at a level of 19 km/wk at 40 to 55% of peak V(O2) is sufficient to increase aerobic fitness levels, and increasing either exercise intensity or the amount beyond these parameters will yield additional separate and combined effects on markers of aerobic fitness. Therefore, it is appropriate to recommend mild exercise to improve fitness and reduce cardiovascular risk yet encourage higher intensities and amounts for additional benefit.

Adult↗

PubMed2005

A comparison of methods for estimating the lactate threshold.

The purpose of this study was to examine the accuracy of tests that may be used by distance runners to estimate the lactate threshold. Competitive distance runners/triathletes (N = 27) performed a criterion test that directly measured (blood lactate of 4.0 mmol.L(-1)) the lactate threshold. Subjects then performed 4 tests (VDOT, 3,200-m time trial, 30-minute time trial, Conconi) that estimate the threshold. Mean estimations of the running velocity at the lactate threshold from the 30-minute time trial (standard error of the estimate, SEE, 0.21 m.s(-1)) and VDOT (SEE 0.41 m.s(-1)) methods did not differ (P>0.05) from the criterion. In terms of heart rate, the 30-minute time trial estimation did not significantly differ (SEE 8.0 b.min(-1)) from criterion. These findings suggest that the 30-minute time-trial method should be considered by coaches and distance runners/triathletes as a method for estimating both the running velocity and heart rate at the lactate threshold.

Adult↗

PubMed2005

Proteome analysis of skeletal muscle from obese and morbidly obese women.

Obesity-related diseases such as the metabolic syndrome and type 2 diabetes originate, in part, from the progressive metabolic deterioration of skeletal muscle. A preliminary proteomic survey of rectus abdominus muscle detected a statistically significant increase in adenylate kinase (AK)1, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and aldolase A in obese/overweight and morbidly obese women relative to lean control subjects. AK1 is essential for the maintenance of cellular energy charge, and GAPDH and aldolase A are well known glycolytic enzymes. We found that muscle AK1 protein and enzymatic activity increased 2.9 and 90%, respectively, in obese women and 9.25 and 100%, respectively, in morbidly obese women. The total enzymatic activity of creatine kinase, which also regulates energy metabolism in muscle, was shown to increase 30% in obese/overweight women only. We propose that increased protein and enzymatic activity of AK1 is representative of a compensatory glycolytic drift to counteract reduced muscle mitochondrial function with the progression of obesity. This hypothesis is supported by increased abundance of the glycolytic enzymes GAPDH and aldolase A in obese and morbidly obese muscle. In summary, proteome analysis of muscle has helped us better describe the molecular etiology of obesity-related disease.

Adenylate Kinase↗

PubMed2004

Exercise training increases electron and substrate shuttling proteins in muscle of overweight men and women with the metabolic syndrome.

Aerobic conditioned muscle shows increased oxidative metabolism or glucose relative to untrained muscle at a given absolute exercise intensity. The studies of a targeted risk reduction intervention through defined exercise (STRRIDE) study is an aerobic exercise intervention in men and women with features of metabolic syndrome (Kraus WE, Torgan CE, Duscha BD, Norris J, Brown SA, Cobb FR, Bales CW, Annex BH, Samsa GP, Houmard JA, and Slentz CA, Med Sci Sports Exerc 33: 1774-1784, 2001), with four muscle biopsies taken during training and detraining time points. Here, we expanded a previous study (Hittel DS, Kraus WE, and Hoffman EP, J Physiol 548: 401-410, 2003) and used mRNA profiling to investigate gene transcripts associated with energy and substrate metabolism in STRRIDE participants. We found coordinate regulation of key metabolic enzymes with aerobic training in metabolic syndrome (aspartate aminotransferase 1, lactate dehydrogenase B, and pyruvate dehydrogenase-alpha(1)). All were also quickly downregulated by detraining, although the induction was not an acute response to activity. Protein and enzymatic assays were used to validate mRNA induction with aerobic training and loss with detraining (96 h to 2 wk) in 10 male and 10 female STRRIDE subjects. We propose that training coordinately increases the levels of aspartate aminotransferase 1, lactate dehydrogenase B, and pyruvate dehydrogenase-alpha(1) subunit, increasing glucose metabolism in muscle by liberating pyruvate for oxidative metabolism and, therefore, limiting lactate efflux. Serial measurement of fasting plasma lactate from 62 subjects from the same exercise group demonstrated a significant decrease of circulating lactate with training. We also found evidence for sex-specific molecular remodeling of muscle with ubiquinol-cytochrome c reductase core protein II, a component of mitochondrial respiratory complex III, which showed an increase after training that was specific to women. These biochemical adaptations complement existing molecular models for improved glucose tolerance with exercise intervention in prediabetic individuals.

Adult↗

PubMed2004

Effects of the amount of exercise on body weight, body composition, and measures of central obesity: STRRIDE--a randomized controlled study.

BACKGROUND: Obesity is a major health problem due, in part, to physical inactivity. The amount of activity needed to prevent weight gain is unknown. OBJECTIVE: To determine the effects of different amounts and intensities of exercise training. DESIGN: Randomized controlled trial (February 1999-July 2002). SETTING AND PARTICIPANTS: Sedentary, overweight men and women (aged 40-65 years) with mild to moderate dyslipidemia were recruited from Durham, NC, and surrounding communities. INTERVENTIONS: Eight-month exercise program with 3 groups: (1) high amount/vigorous intensity (calorically equivalent to approximately 20 miles [32.0 km] of jogging per week at 65%-80% peak oxygen consumption); (2) low amount/vigorous intensity (equivalent to approximately 12 miles [19.2 km] of jogging per week at 65%-80%), and (3) low amount/moderate intensity (equivalent to approximately 12 miles [19.2 km] of walking per week at 40%-55%). Subjects were counseled not to change their diet and were encouraged to maintain body weight. MAIN OUTCOME MEASURES: Body weight, body composition (via skinfolds), and waist circumference. RESULTS: Of 302 subjects screened, 182 met criteria and were randomized and 120 completed the study. There was a significant (P<.05) dose-response relationship between amount of exercise and amount of weight loss and fat mass loss. The high-amount/vigorous-intensity group lost significantly more body mass (in mean [SD] kilograms) and fat mass (in mean [SD] kilograms) (-2.9 [2.8] and -4.8 [3.0], respectively) than the low-amount/moderate-intensity group (-0.9 [1.8] and -2.0 [2.6], respectively), the low-amount/vigorous-intensity group (-0.6 [2.0] and -2.5 [3.4], respectively), and the controls (+1.0 [2.1] and +0.4 [3.0], respectively). Both low-amount groups had significantly greater improvements than controls but were not different from each other. Compared with controls, all exercise groups significantly decreased abdominal, minimal waist, and hip circumference measurements. There were no significant changes in dietary intake for any group. CONCLUSIONS: In nondieting, overweight subjects, the controls gained weight, both low-amount exercise groups lost weight and fat, and the high-amount group lost more of each in a dose-response manner. These findings strongly suggest that, absent changes in diet, a higher amount of activity is necessary for weight maintenance and that the positive caloric imbalance observed in the overweight controls is small and can be reversed by a modest amount of exercise. Most individuals can accomplish this by walking 30 minutes every day.

Adult↗

PubMed2004

Gender and racial differences in lipoprotein subclass distributions: the STRRIDE study.

Recent research has focused on the potential atherogenicity of various lipoprotein subclasses and their link to coronary heart disease (CHD) risk. This investigation seeks to identify differences in lipoprotein subclass distributions among a biracial, middle-aged population, while controlling for a number of confounding risk factors. Fasting plasma samples were analyzed in 285 sedentary, mildly dyslipidemic, overweight individuals between 40 and 65 years with no known history of CHD or diabetes. Women had lower levels of small and medium LDL, medium VLDL, large VLDL, and small HDL with a much higher concentration of large HDL than men. Whites had significantly more IDL, small LDL, medium VLDL, and large VLDL with lower levels of large LDL than blacks. HDL and LDL size were larger among blacks and women; VLDL size was greater among whites and men. There was also a trend for men to have more LDL particles than women and whites to have a higher LDL particle concentration than blacks. Within this homogenous population, there were distinct differences between gender and racial groups. Blacks and women had less atherogenic profiles than whites and men, which was not evident from the standard lipid panel.

Adult↗

PubMed2004

Weight loss and exercise: implications for muscle lipid metabolism and insulin action.

Implications for Muscle Lipid Metabolism and An accumulation of intramuscular lipid has been reported with obesity and linked with insulin resistance. The purpose of this paper is to discuss: 1) mechanisms that may be responsible for intramuscular lipid accumulation with obesity, and 2) the effects of common interventions (weight loss or exercise) for obesity on skeletal muscle lipid metabolism and intramuscular lipid content. Data suggest that the skeletal muscle of morbidly obese humans is characterized by the preferential partitioning of lipid toward storage rather than oxidation. This phenotype may, in part, contribute to increased lipid deposition in both muscle and adipose tissue, and promote the development of morbid obesity and insulin resistance. Weight loss intervention decreases intramuscular lipid content, which may contribute to improved insulin action. On the other hand, exercise training improves insulin action and increases fatty acid oxidation in the skeletal muscle of obese/morbidly obese individuals. In summary, the accumulation of intramuscular lipid appears to be detrimental in terms of inducing insulin resistance; however, the accumulation of lipid can be reversed with weight loss. The mechanism(s) by which exercise enhances insulin action remains to be determined.

Exercise↗