The thermic effect of food at rest, during 30 min of cycle exercise, and postexercise with two sequences of exercise and meal (before or after exercise) was compared in eight lean (mean +/- SE, 12.8 +/- 0.7% body fat) and eight obese men (29.7 +/- 0.6% fat) to determine whether exercise before or after a meal enhances thermogenesis. The groups were matched for age, height, and lean body mass (LBM) in order to study the relationship between thermogenesis and body fat independent of LBM. Metabolic rate was measured by indirect calorimetry on five mornings, in randomized order, after an overnight fast. Treatments on respective days were 1) 3-h rest, no meal; 2) 3-h rest after a 750-kcal mixed meal (14% protein, 31% fat, 55% carbohydrate); 3) during and 3 h after 30 min of cycling, no meal; 4) during and 3 h after 30 min of cycling, meal 30 min before exercise; and 5) 3 h after 30 min of cycling, meal immediately after exercise. The thermic effect of food, which is the fed minus fasted caloric expenditure, was significantly greater for the lean than the obese men under the resting (mean +/- SE 53 +/- 5 vs. 26 +/- 5 kcal over 3 h for the lean and obese groups, P less than 0.01), exercise (26 +/- 4 vs. 4 +/- 2 kcal over 30 min, P less than 0.01), and both postexercise conditions. However, for the lean men the thermic effect of food was significantly greater for the meal-before-exercise than the resting and the meal-after-exercise conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
In the absence of a ⩒o2-work-rate plateau, debate continues regarding the best way to verify that the peak ⩒o2 achieved during incremental exercise (⩒o2peak) is the "true ⩒o2max." Oft-used "secondary criteria" have been questioned in conjunction with the contention that a severe-intensity constant-work-rate "verification bout" should be considered the "gold standard." The purpose of this study was to compare the ⩒o2peak during ramp incremental cycling (RAMP-INC) by a heterogeneous (with respect to body composition and sex) cohort of sedentary individuals with the ⩒o2peak during severe-intensity constant-work-rate cycling (CWR) performed after RAMP-INC at the highest work rate achieved. A secondary purpose was to determine the degree to which traditional and newly-proposed age-dependent secondary criteria (RER, HR) identified RAMP-INC which CWR confirmed were characterized by a submaximal ⩒o2peak. Thirty-five healthy male (n = 19: 33.4 ± 6.3 yrs) and female (26.8 ± 3.6 yrs) sedentary participants performed RAMP-INC followed by CWR. The ⩒o2peak values from the two tests were correlated (r = 0.96; p < 0.01; mean CV = 24%); however, ⩒o2peak for CWR was significantly greater (29.6 ± 7.2 v. 28.6 ± 6.8 mL∙min-1∙kg-1; p < 0.01) with a mean bias of 0.98 mL∙min-1∙kg-1 (z = -2.9, p < 0.01). Both traditional and newly-proposed criterion values for RER were achieved during RAMP-INC by 33 of 35 participants (including 21 of 23 who registered a higher ⩒o2peak on CWR). The traditional HR criterion value was achieved on only seven tests (three of which were confirmed to be characterized by a submaximal ⩒o2peak) while use of less stringent newly-proposed criteria resulted in acceptance of an additional seven tests of which five were confirmed to be submaximal. Severe-intensity CWR to limit of tolerance indicates that RAMP-INC underestimates ⩒o2max in sedentary individuals and both traditional and newly-proposed secondary criteria are ineffective for identifying such tests.
Background A large proportion of HIV-infected patients on antiretroviral medication develop insulin resistance, especially in the context of fat redistribution. This study investigates the interrelationships among fat distribution, hepatic lipid content, and insulin resistance in HIV-infected men. Methods We performed a cross-sectional analysis of baseline data from 23 HIV-infected participants in three prospective clinical studies. Magnetic resonance spectroscopy was used to quantify hepatic lipid concentrations. Magnetic resonance imaging was used to quantify whole-body adipose tissue compartments: that is, subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) volumes, as well as the intermuscular adipose tissue (IMAT) subcompartment and the omental-mesenteric adipose tissue (OMAT) and retroperitoneal adipose tissue (RPAT) subcompartments of VAT. The homeostasis model for assessment of insulin resistance (HOMA-IR) was calculated from fasting glucose and insulin concentrations. Results Hepatic lipid content correlated significantly with total VAT (r=0.62, P=0.0014), but not with SAT (r=0.053, P=0.81). In univariate analysis, hepatic lipid content was associated with the OMAT (r=0.67, P=0.0004) and RPAT (r=0.53, P=0.009) subcompartments; HOMA-IR correlated with both VAT and hepatic lipid contents (r=0.61, P=0.057 and r=0.68, P=0.0012, respectively). In stepwise linear regression models, hepatic lipid had the strongest associations with OMAT and with HOMA-IR. Conclusion Hepatic lipid content is associated with VAT volume, especially the OMAT subcompartment, in HIV-infected men. Hepatic lipid content is associated with insulin resistance in HIV-infected men. Hepatic lipid content might mediate the relationship between VAT and insulin resistance among treated, HIV-infected men.
The lipodystrophy syndrome (adipose tissue redistribution and metabolic abnormalities) observed with highly active antiretroviral therapy (HAART) during human immunodeficiency virus (HIV) infection may be related to increased proinflammatory cytokine activity. We measured acute cytokine (TNF-alpha, IL-6, leptin), glycerol, and lactate secretion from abdominal subcutaneous adipose tissue (SAT), and systemic cytokine levels, in HIV-infected subjects with and without lipodystrophy (HIVL+ and HIVL-, respectively) and healthy non-HIV controls. Lipodystrophy was confirmed and characterized as adipose tissue redistribution in HIVL+ compared with HIVL- and controls, by dual-energy X-ray absorptiometry and by whole body MRI. TNF-alpha secretion from abdominal SAT and circulating levels of IL-6, soluble TNF receptors I and II, and insulin were elevated in HIVL+ relative to HIVL- and/or controls, particularly in HIVL+ undergoing HAART. In the HIV-infected group as a whole, IL-6 secretion from abdominal SAT and serum IL-6 were positively associated with visceral fat and were negatively associated with the relative amount of lower limb adipose tissue (P < 0.01). Decreased leptin and increased lactate secretion from abdominal SAT were specifically associated with HAART. In conclusion, increased cytokine secretion from adipose tissue and increased systemic proinflammatory cytokine activity may play a significant role in the adipose tissue remodeling and/or the metabolic abnormalities associated with the HIV-lipodystrophy syndrome in patients undergoing HAART.
Introduction: Type 2 diabetes (T2D) is associated with worse outcomes in various medical conditions. While some studies have shown an increased incidence of acute pancreatitis (AP) in patients with T2D due to higher incidence of cholelithiasis in patients with obesity, others have detected a paradoxical effect on mortality. The aim of this study was to further explore the impact of T2D on outcomes in AP. Methods: This was a retrospective cohort study using the 2013 National Inpatient Sample, the largest publically available inpatient database in the US. All patients with an ICD-9 CM code for a principal diagnosis of AP were included. There were no exclusion criteria. The primary outcome was in-hospital mortality. Secondary outcomes were morbidity measured by intensive care unit (ICU) admission, shock and multi-organ failure, resource utilization measured by abdominal CT scan, abdominal ultrasound (US), total parenteral nutrition (TPN) use, length of hospital stay (LOS), and total hospitalization charges (THC). Patients were classified as having or not having T2D, stratified by organ failure, using ICD-9 CM codes. Using multivariate regression analysis, odds ratios and means were adjusted for: age; sex; race; median income in the patient's zip code; Charlson Comorbidity Index; hospital region; urban location; size and teaching status.Table 2Results: 257,405 patients with acute pancreatitis were included in the study, 77,365 (30%) of whom had a T2D. Mean age was 53 years and 44% were female. The overall mortality was 0.7% (0.9% in patients with T2D). On multivariate analysis, the odds of in-hospital mortality of patients with AP and T2D were less when compared to patients without T2D (OR:0.65, 95%CI:0.51-0.83,p < 0.01). Table 1 shows adjusted odds ratios, adjusted means and p-values. Looking at morbidity as measured by shock, need for ICU admission, and end-organ damage, there was no statistically significant difference between patients with T2D and AP as opposed to patients without diabetes. Also, no significant differences were found in terms of length of stay, THC, TPN or abdominal imaging use.Table 1Conclusion: For patients with a principal diagnosis of AP, the coincident diagnosis of T2D is associated with lesser in-hospital mortality rates compared to patients without T2D, which may suggest an effect of the known “obesity paradox”, as most patients with T2D are obese. T2D does not affect morbidity, inpatient resource utilization, THC or hospital LOS in patients with AP.
OBJECTIVE To determine the impact of a health system–wide primary care diabetes management system, which included targeted guidelines for type 2 diabetes (T2DM) and prediabetes (dysglycemia) screening, on detection of previously undiagnosed dysglycemia cases. RESEARCH DESIGN AND METHODS Intervention included electronic health record (EHR)–based decision support and standardized providers and staff training for using the American Diabetes Association guidelines for dysglycemia screening. Using EHR data, we identified 40,456 adults without T2DM or recent screening with a face-to-face visit (March 2011–December 2013) in five urban clinics. Interrupted time series analyses examined the impact of the intervention on trends in three outcomes: 1) monthly proportion of eligible patients receiving dysglycemia testing, 2) two negative comparison conditions (dysglycemia testing among ineligible patients and cholesterol screening), and 3) yield of undiagnosed dysglycemia among those tested. RESULTS Baseline monthly proportion of eligible patients receiving testing was 7.4–10.4%. After the intervention, screening doubled (mean increase + 11.0% [95% CI 9.0, 13.0], proportion range 18.6–25.3%). The proportion of ineligible patients tested also increased (+5.0% [95% CI 3.0, 8.0]) with no concurrent change in cholesterol testing (+0% [95% CI −0.02, 0.05]). About 59% of test results in eligible patients showed dysglycemia both before and after the intervention. CONCLUSIONS Implementation of a policy for systematic dysglycemia screening including formal training and EHR templates in urban academic primary care clinics resulted in a doubling of appropriate testing and the number of patients who could be targeted for treatment to prevent or delay T2DM.
Dietary components have potential to arrest or modify chronic disease processes including obesity, cancer, and comorbidities. However, clinical research to translate mechanistic nutrition data into clinical interventions is needed. We have developed a one-year transitional postdoctoral curriculum to prepare nutrition scientists in the language and practice of medicine and in clinical research methodology before undertaking independent research. Candidates with an earned doctorate in nutrition science receive intensive, didactic training at the interface of nutrition and medicine, participate in supervised medical observerships, and join ongoing clinical research. To date, we have trained four postdoctoral fellows. Formative evaluation revealed several learning barriers to this training, including deficits in prior medical science knowledge and diverse perceptions of the role of the translational nutrition scientist. Several innovative techniques to address these barriers are discussed. We propose the fact that this “train the trainer” approach has potential to create a new translational nutrition researcher competent to identify clinical problems, collaborate with clinicians and researchers, and incorporate nutrition science across disciplines from “bench to bedside.” We also expect the translational nutrition scientist to serve as an expert resource to the medical team in use of nutrition as adjuvant therapy for the prevention and management of chronic disease.
Skeletal muscle (SM) is a large and physiologically important compartment. Adipose tissue is found interspersed between and within SM groups and is referred to as intermuscular adipose tissue (IMAT). The study objective was to develop prediction models linking appendicular lean soft tissue (ALST) estimates by dual-energy X-ray absorptiometry (DXA) with whole body IMAT-free SM quantified by magnetic resonance imaging. ALST and total-body IMAT-free SM were evaluated in 270 healthy adults [body mass index (BMI) of <35 kg/m 2 ]. The SM prediction models were then validated by the leave-one-out method and by application in a new group of subjects who varied in SM mass [anorexia nervosa (AN), n = 23; recreational athletes, n = 16; patients with acromegaly, n = 7]. ALST alone was highly correlated with whole body IMAT-free SM [ model 1: R 2 = 0.96, standard error (SE) = 1.46 kg, P < 0.001]; age ( model 2: R 2 = 0.97, SE = 1.38 kg, P < 0.001) and sex and race ( model 3: R 2 = 0.97, SE = 1.06 kg, both P < 0.001) added significantly to the prediction models. All three models validated in the athletes and patients with acromegaly but significantly ( P < 0.01–0.001) over-predicted SM in the AN group as a whole. However, model 1 was validated in AN patients with BMIs in the model-development group range ( n = 11; BMI of >16 kg/m 2 ) but not in those with a BMI of <16 kg/m 2 ( n = 12). The DXA-based models are accurate for predicting IMAT-free SM in selected populations and thus provide a new opportunity for quantifying SM in physiological and epidemiological investigations.