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ABSTRACT: Undetectable = Untransmittable (U=U) is a key message emphasizing that antiretroviral therapy suppresses HIV and prevents its sexual transmission. However, dissemination of U=U varies among health care providers, potentially leading to knowledge gaps among patients. Little research exists on the understanding of U=U among active duty men who have sex with men (MSM) in the U.S. military. Our cross-sectional, online study examines 222 active duty MSM to determine prevalence of accurate knowledge of U=U and demographic predictors of misinformation. Participants received a pre-exposure prophylaxis (PrEP) overview and were asked to indicate if the statement "Undetectable equals Untransmittable" was true or false. Although the majority accurately understood U=U (70%; n = 156), approximately 30% did not (n = 66); a binary logistic regression revealed lower U=U understanding among White, bisexual, unmarried, and Marines/Navy participants. Standardized education on U=U is crucial for resolving knowledge gaps and combating stigmas surrounding HIV treatment.

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INTRODUCTION: Men who have sex with men (MSM) account for over half of new diagnoses of human immunodeficiency virus (HIV) every year in the United States, with over one-third of this population being unaware of their HIV status. The U.S. Military requires biannual HIV testing for all service members. Although this may be an appropriate recommendation for the military at large, current health protection agencies suggest more frequent testing for those at increased risk of HIV transmission, such as those in the MSM community. However, more frequent testing for those at higher risk relies heavily on the preliminary step of patient disclosure of sexual practices to health care providers. MATERIALS AND METHODS: An exploratory cross-sectional study was conducted in order to gain a better understanding of the relationship between sexual health variables and the disclosure of sexual identity to health care providers by MSM service members. A convenience sample of MSM currently serving in the U.S. military services (N = 354) was used to collect demographic data, sexual health and history, and opinions concerning medical treatment and HIV. Analyses of the data were conducted using univariate analysis and multivariate regression. RESULTS: Men of color were more likely to report a higher degree of sexual identification transparency with their health care providers, which deviates from the civilian population. Pre-exposure prophylaxis (PrEP) uptake was increased among individuals who were more transparent with their health care providers. CONCLUSIONS: Findings from this study indicate that feeling more comfortable sharing one's sexual identification with a health care provider results in increased engagement with HIV prevention measures. Potential implications for the Military Health System are the advancement of preventive sexual health screening procedures and the development and revision of policies that promote positive outcomes for gender and sexual minorities.

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The HEALTHY study was a randomized, controlled, multicenter and middle school-based, multifaceted intervention designed to reduce risk factors for the development of type 2 diabetes. The study randomized 42 middle schools to intervention or control, and followed students from the sixth to the eighth grades. Here we describe the design of the HEALTHY nutrition intervention component that was developed to modify the total school food environment, defined to include the following: federal breakfast, lunch, after school snack and supper programs; a la carte venues, including snack bars and school stores; vending machines; fundraisers; and classroom parties and celebrations. Study staff implemented the intervention using core and toolbox strategies to achieve and maintain the following five intervention goals: (1) lower the average fat content of foods, (2) increase the availability and variety of fruits and vegetables, (3) limit the portion sizes and energy content of dessert and snack foods, (4) eliminate whole and 2% milk and all added sugar beverages, with the exception of low fat or nonfat flavored milk, and limit 100% fruit juice to breakfast in small portions and (5) increase the availability of higher fiber grain-based foods and legumes. Other nutrition intervention component elements were taste tests, cafeteria enhancements, cafeteria line messages and other messages about healthy eating, cafeteria learning laboratory (CLL) activities, twice-yearly training of food service staff, weekly meetings with food service managers, incentives for food service departments, and twice yearly local meetings and three national summits with district food service directors. Strengths of the intervention design were the integration of nutrition with the other HEALTHY intervention components (physical education, behavior change and communications), and the collaboration and rapport between the nutrition intervention study staff members and food service personnel at both school and district levels.

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New pharmacologic agents are being sought to help manage the epidemic of obesity and its consequences. Understanding the challenges of the history of obesity drugs is wise before investing in new obesity agents. Expectations of patients, physicians, and drug company executives are not consistent with characteristics of current agents or most potential new ones. Owing to the complex biology underlying body weight regulation, combinations of agents may be necessary to improve weight loss efficacy.

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Recent studies suggest that leptin may be an important metabolic signal for energy regulation in rodents, but the role of leptin in human energy regulation remains uncertain. Because adaptive variations in energy expenditure play an important role in human energy regulation, we investigated the relationship between leptin and energy expenditure parameters in 61 weight-stable men and women aged 18 years to 81 years who were not obese. Measurements were made of circulating leptin in the fasting state, body fat and fat free mass, resting metabolic rate (n = 61), free-living total energy expenditure (n = 52), and the thermic effect of feeding (n = 33). After statistically accounting for age, body fat, and fat free mass, there was no association between leptin and any measured energy expenditure parameter. In addition, there was no effect of age on the relationship between circulating leptin and body fat mass. These results indicate that physiological variations in circulating leptin are not linked with adaptive variations in energy expenditure in humans, in contrast to indications of this phenomenon in the ob/ob mouse.

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Leptin's association with fasting insulin raises the possibility that hyperleptinaemia is an additional component of the Metabolic Syndrome, or perhaps underlies the syndrome. This population-based study of Western Samoans examined the relationship of serum leptin with insulin sensitivity assessed by Homeostatic Model Assessment (HOMA) and components of the Metabolic Syndrome. Two hundred and forty subjects (114 men, 126 women), aged 28-74 years, were drawn from a study conducted in 1991. An oral glucose tolerance test indicated that 59 subjects had diabetes. Diabetic men had higher leptin levels than non-diabetic (6.0 vs 3.2 ng ml-1) but this difference was no longer significant after adjustment for BMI. Leptin levels in diabetic women (24.7 ng ml-1) non-diabetic women (22.6 ng ml-1) were not different. Leptin was strongly, positively correlated with BMI, fasting insulin and mean blood pressure after adjusting for age and sex (r > 0.43, p < 0.001), irrespective of glucose tolerance status. Linear regression models indicated that leptin was associated with insulin sensitivity independent of age, BMI, waist/hip ratio, triglycerides, HDL-cholesterol, and hypertension. Similar models were computed with mean blood pressure or triglycerides as the dependent variable, and including insulin sensitivity with the independent variables. Leptin was independently associated with mean blood pressure in men, but was not independently associated with triglycerides. Mean levels of 2-h insulin, triglycerides, LDL-cholesterol, and systolic blood pressure varied across tertiles of leptin in men after adjusting for age, BMI, and insulin sensitivity, and mean levels in the top tertile tended to be higher than in the lowest tertile. These results indicate an independent relationship between leptin and insulin sensitivity, but the equivocal results concerning associations of leptin with components of the Metabolic Syndrome make it unlikely that leptin affects these directly.

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OBJECTIVE: To measure serum leptin concentrations in the Polynesian population of Western Samoa and to examine epidemiological associations of leptin with anthropometric, demographic, behavioural, and metabolic factors in this population with a high prevalence of obesity and non-insulin dependent diabetes mellitus. DESIGN: Cross sectional study, leptin concentration being measured in a subgroup of a population based sample. SUBJECTS: 240 Polynesian men and women aged 28-74 years were selected to cover the full range of age, body mass index, and glucose tolerance. MAIN OUTCOME MEASUREMENTS: Serum leptin, insulin, and glucose concentrations; anthropometric measures; physical activity; and area of residence. RESULTS: Leptin concentrations were correlated with body mass index (r = 0.80 in men, 0.79 in women) and waist circumference (r = 0.82 in men, 0.78 in women) but less so with waist to hip ratio. At any body mass index, leptin concentration was higher in women than men (geometric mean adjusted for body mass index 15.3 v 3.6 pg/l, P < 0.001). Leptin concentration also correlated with fasting insulin concentration (r = 0.63 in men, 0.64 in women) and insulin concentration 2 hours after a glucose load (r = 0.58 in men, 0.52 in women). These associations remained significant after controlling for body mass index; effects of physical activity and of rural or urban living on leptin concentration were eliminated after adjusting for obesity, except values remained high in urban men. 78% of variance in leptin was explained by a model including fasting insulin concentration, sex, body mass index, and a body mass index by sex interaction term. Similar results were obtained if waist circumference replaced body mass index. CONCLUSIONS: The strong relation of leptin with obesity is consistent with leptin production being proportional of mass to adipose tissue. The relation with insulin independent of body mass index suggests a possible role for leptin in insulin resistance or hyperinsulinaemia.

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BACKGROUND: Decreased insulin secretion may contribute to the deterioration of glucose tolerance associated with aging. METHODS: We studied the insulin response to a 3-hour hyperglycemic clamp (10 mM) of 19 young (24 +/- 1 y) subjects with normal glucose tolerance and 60 older (65 +/- 1 y) subjects with various levels of glucose tolerance. RESULTS: The noninsulin dependent diabetic (NIDDM) group had a diminished first phase immunoreactive (IR)-insulin response compared to young and nondiabetic older groups (p < .05). The older groups had a lower rate of change in IR insulin concentration during the third hour of hyperglycemia compared to the young group (p < .05). This was not, however, a universal finding, because a decreased third hour response was not seen in a subgroup of older subjects whose glucose tolerance was similar to that of the young group. Another subgroup of older subjects with a decrease in glucose tolerance mild enough to be considered normal by the National Diabetes Group Criteria tended to have both an increase in the early insulin response and a decrease in the third hour response. More severe decreases in glucose tolerance were associated with blunting of the early response. CONCLUSION: Aberrations in early and late phase glucose-stimulated insulin responses appear to be present in older subjects with even mildly decreased glucose tolerance. Some individuals, however, show no evidence of deterioration of glucose tolerance or insulin response to glucose with aging, at least up to age 70 years.

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Studies have shown that insulin resistance increases with age, independent of changes in total adiposity. However, there is growing evidence that the development of insulin resistance may be more closely related to abdominal adiposity. To evaluate the independent effects of aging and regional and total adiposity on insulin resistance, we performed hyperinsulinemic euglycemic clamps on 17 young (21-33 yr) and 67 older (60-72 yr) men and women. We assessed FFM and total and regional adiposity by hydrodensitometry and anthropometry. Insulin-stimulated GDRs at a plasma insulin concentration of approximately 450 pM averaged 45.6 +/- 3.3 mumol.kg FFM-1 x min-1 (mean +/- SE) in the young subjects, 45.6 +/- 10.0 mumol.kg FFM-1 x min-1 in 24 older subjects who were insulin sensitive, and 23.9 +/- 11.7 mumol.kg FFM-1 x min-1 in 43 older subjects who were insulin resistant. Few significant differences were apparent in skin-fold and circumference measurements between young and insulin-sensitive older subjects, but measurements at most central body sites were significantly larger in the insulin-resistant older subjects. Waist girth accounted for > 40% of the variance in insulin action, whereas age explained only 10-20% of the total variance and < 2% of the variance when the effects of waist circumference were statistically controlled. These results suggest that insulin resistance is more closely associated with abdominal adiposity than with age.

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To study the effect of acute exercise on caloric intake in normal-weight young people, food intake was monitored in 10 men and 10 women during consecutive 5-d periods, one with and one without exercise. Food intake during the exercise period was compared with that during the control period. Caloric intake during the control period was 2467 +/- 165 kcal/d (means +/- SEM) for men and 1831 +/- 103 kcal/d for women. During the exercise period the men increased their caloric intake to 2658 +/- 188 kcal/d and the women's caloric intake remained unchanged, 1830 +/- 91 kcal/d. Caloric intake was not affected by sequence of treatment or duration of protocol. Men responded to 5 d of acute exercise with increased caloric intake (208 +/- 64 kcal/d), which was insufficient to compensate for the caloric cost of exercise (596 kcal/d above resting metabolic rate). Women did not change their caloric intake despite expending 382 kcals/d during exercise. Consequently, both normal-weight men and women were in negative caloric balance during the exercise period.

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The effects of a single bout of exercise to exhaustion on pancreatic insulin secretion were determined in seven untrained men by use of a 3-h hyperglycemic clamp with plasma glucose maintained at 180 mg/100 ml. Clamps were performed either 12 h after an intermittent treadmill run at approximately 77% maximum O2 consumption or without prior exercise. Arterialized blood samples for glucose, insulin, and C-peptide determination were obtained from a heated hand vein. The peak insulin response during the early phase (0-10 min) of the postexercise clamp was higher (81 +/- 8 vs. 59 +/- 9 microU/ml; P less than 0.05) than in the nonexercise clamp. Incremental areas under the insulin (376 +/- 33 vs. 245 +/- 51 microU.ml-1.min) and C-peptide (17 +/- 2 vs. 12 +/- 1 ng.ml-1.min) curves were also greater (P less than 0.05) during the early phase of the postexercise clamp. No differences were observed in either insulin concentrations or whole body glucose disposal during the late phase (15-180 min). Area under the C-peptide curve was greater during the late phase of the postexercise clamp (650 +/- 53 vs. 536 +/- 76 ng.ml-1.min, P less than 0.05). The exercise bout induced muscle soreness and caused an elevation in plasma creatine kinase activity (142 +/- 32 vs. 305 +/- 31 IU/l; P less than 0.05) before the postexercise clamp. We conclude that in untrained men a bout of running to exhaustion increased pancreatic beta-cell insulin secretion during the early phase of the hyperglycemic clamp. Increased insulin secretion during the late phase of the clamp appeared to be compensated by increased insulin clearance.

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Insulin secretion in response to glucose stimulation is reduced in endurance-trained humans. In this study, a modified hyperglycemic clamp, with a superimposed arginine infusion and fat meal, was performed on eight endurance-trained and nine untrained men to determine whether insulin secretory capacity is reduced by exercise training. Raising the plasma glucose concentration to approximately 450 mg/dl resulted in a plasma insulin response in the trained men that was approximately 64% lower than that of the untrained (peak values: 54 +/- 8 vs. 149 +/- 35 microU/ml; P less than 0.001). When a primed continuous infusion of arginine was superimposed on the hyperglycemia, the plasma insulin response was also markedly lower (66%) in the trained subjects, reaching peak values of 333 +/- 68 and 974 +/- 188 microU/ml for trained and untrained subjects, respectively (P less than 0.005). When insulin secretion was further stimulated during the arginine-infused hyperglycemia by the ingestion of a high-fat meal, peak insulin concentrations averaged 989 +/- 205 microU/ml in the trained compared with 2,232 +/- 455 microU/ml in the untrained subjects (P less than 0.01). The response of gastric inhibitory polypeptide (GIP) to the fat meal was delayed and blunted, suggesting that some enteric factor(s) other than GIP mediated the insulinotropic effect of the fat meal. The reduced plasma insulin response in trained people to the stimuli investigated suggests that regular exercise produces either several adaptations within the beta-cell or a single alteration of the beta-cell that results in an attenuation of the insulin secretory response to glucose, arginine, and fat ingestion.

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High plasma levels of HDL2, a subfraction of high-density lipoprotein (HDL) cholesterol, are associated with a reduced risk of coronary heart disease. To investigate the characteristics related to HDL2 cholesterol levels, we measured lipoprotein levels and several metabolic and anthropometric variables in 146 healthy subjects (77 men and 69 women) in the seventh decade of life. The level of HDL2 cholesterol was inversely correlated with the ratio of the waist-to-hip circumference (r = -0.335 for men; r = -0.370 for women; P less than 0.01) and the plasma insulin level (r = -0.400 for men; r = -0.398 for women; P less than 0.001). In a multiple regression model including both sexes, 41 percent of the variance in the HDL2 level was explained by the combined effect of the waist-to-hip ratio (P less than 0.0001), the plasma insulin level (P = 0.0003), and the degree of glucose tolerance indicated by the integrated area under the plasma glucose curve after an oral glucose-tolerance test (P = 0.05). The body-mass index, total percentage of body fat, maximal oxygen uptake, diet, and sex were not significant predictors of the HDL2 level when added to this model, whereas the original variables remained significant predictors. The HDL2 cholesterol level in subjects at the 25th percentile for waist-to-hip ratio was 153 percent of that in subjects at the 75th percentile. We conclude that HDL2 levels are inversely correlated with truncal fat, plasma insulin levels, and the presence of glucose intolerance and are not independently associated with sex or total body fat.

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Epinephrine's effect to increase metabolic rate is accompanied by changes in the plasma concentrations of insulin, glucagon, and metabolic substrates. Because both glucagon and insulin have been reported to affect thermogenesis, these hormones might contribute to or modify the thermogenic response to epinephrine. To determine if the epinephrine-induced increase in metabolic rate is secondary to changes in glucagon or insulin or to changes in the fuels modulated by these hormones, metabolic rate was measured by indirect calorimetry in five normal weight post-absorptive young men on three occasions: study A, an intravenous epinephrine infusion alone; study B, a 4-h "islet clamp" consisting of somatostatin infusion with basal insulin and glucagon replacement; and study C, an intravenous epinephrine infusion combined with the islet clamp. A 1-h base-line period preceded 2 h of epinephrine infusion. During the 4-h islet clamp (study B), metabolic rate and plasma concentrations of epinephrine, insulin, glucagon, and glucose remained unchanged. During the infusion of epinephrine alone (study A), metabolic rate and concentrations of glucagon, free fatty acids, and C-peptide increased as expected. Also as expected, the glycemic response to epinephrine infusion was much larger when insulin and glucagon levels were fixed with the islet clamp (study C). In contrast, the metabolic rate and the free fatty acid concentration responded similarly to epinephrine infusion when insulin and glucagon were fixed (study C) and when they were changing (study A). We conclude that epinephrine increases metabolic rate independently of physiological changes in plasma glucagon or insulin or the circulating fuels they modulate.

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Because of the important role of intra-abdominal fat in predicting increased risk for diabetes, hypertension, and heart disease, methods to quantify intra-abdominal fat are needed. Computed tomography defines quantity of intra-abdominal fat but is associated with significant radiation risk. We explored using magnetic resonance imaging (MRI) to measure amount and distribution of intra-abdominal fat. Because MRI has no known risk, the same subject can be studied repeatedly. Six subjects with percent body fat ranging from 14% to 44% had MRI scans of the chest, abdomen, and thigh on two separate occasions. Total abdominal fat and subcutaneous abdominal fat correlated with percent total body fat as determined from hydrostatic weighing (r = .99, P less than .001). Intra-abdominal fat correlated with the ratio of widest abdominal to widest hip circumference (r = .85, P less than .05). Reproducibility of the MRI measurements of fat was less than 3% for total body areas, less than 5% for subcutaneous fat areas, and less than 10% for internal fat areas. Reproducibility was better in individuals with higher percent total body fat. We conclude that MRI can reliably measure fat areas with no radiation risk to the patient.

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Insulin action is enhanced in people who exercise regularly and vigorously. In the present study, the hyperinsulinemic, euglycemic clamp procedure was used to determine whether this enhanced insulin action is due to an increased sensitivity and/or an increased responsiveness to insulin. To avoid the variability that exists between individuals and complicates cross-sectional studies, the same subjects were studied in the trained exercising state and again after 10 days of physical inactivity. When the plasma insulin concentration was maintained at approximately 78 microU.ml-1 (a submaximal level), glucose disposal rate averaged 8.7 +/- 0.5 mg.kg-1.min-1 before and 6.7 +/- 0.6 mg.kg-1.min-1 after 10 days of activity (P less than 0.001). When the plasma insulin concentration was maintained at approximately 2,000 microU.ml-1 (a maximally effective concentration), the rate of glucose disposal was not significantly different before (15.3 +/- 0.5 mg.kg-1.min-1) compared with after (14.5 +/- 0.4 mg.kg-1.min-1) 10 days without exercise. These results provide evidence that the reversal of enhanced insulin action that occurs within a few days when exercise-trained individuals stop exercising is due to a decrease in sensitivity to insulin, not to a decrease in insulin responsiveness.

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We employed the hyperglycemic clamp technique to investigate the effects of short-term inactivity on insulin secretion in nine (8 men, 1 woman) well-trained subjects. A 3-h hyperglycemic clamp (plasma glucose approximately 180 mg/100 ml) was performed approximately 16 h after a usual training bout and again 14 days after stopping exercise training. There was no significant change in body composition during this short period of inactivity. The mean plasma insulin response to an identical glycemic stimulus was 67% higher after 14 days without exercise (45 +/- 7 after vs. 27 +/- 4 microU/ml before stopping exercise training). Marked increases in the early (0-10 min, 150 +/- 28 vs. 101 +/- 15 microU.ml-1.min) and late (10-180 min, 6,051 +/- 1,257 vs. 3,521 +/- 749 microU.ml-1.min) incremental insulin areas were observed as a result of the physical inactivity. Incremental areas for C-peptide were also elevated significantly in the inactive state for early (12 +/- 2.0 vs. 7 +/- 1 ng.ml-1.min) and late (567 +/- 90 vs. 467 +/- 85 ng.ml-1.min) phases. Urinary excretion of C-peptide increased from 12.1 +/- 1.5 ng/240 min in the exercising state to 21.8 +/- 3.6 ng/240 min in the inactive state. Rates of whole body glucose disposal were not different between exercising and inactive states, indicating a large increase in resistance to the action of insulin. These findings indicate that the decreased insulin secretory response to a glucose stimulus in people who exercise regularly is a relatively short-term effect of exercise.

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To evaluate insulin sensitivity and responsiveness, a two-stage hyperinsulinemic euglycemic clamp procedure (insulin infusions of 40 and 400 mU.m-2.min-1) was performed on 11 endurance-trained and 11 untrained volunteers. A 3-h hyperglycemic clamp procedure (plasma glucose approximately 180 mg/dl) was used to study the insulin response to a fixed glycemic stimulus in 15 trained and 12 untrained subjects. During the 40-mU.m-2.min-1 insulin infusion, the glucose disposal rate was 10.2 +/- 0.5 mg.kg fat-free mass (FFM)-1.min-1 in the trained group compared with 8.0 +/- 0.6 mg.kg FFM-1.min-1 in the untrained group (P less than 0.01). In contrast, there was no significant difference in maximally stimulated glucose disposal: 17.7 +/- 0.6 in the trained vs. 16.7 +/- 0.7 mg.kg FFM-1.min-1 in the untrained group. During the hyperglycemic clamp procedure, the incremental area for plasma insulin was lower in the trained subjects for both early (0-10 min: 140 +/- 18 vs. 223 +/- 23 microU.ml-1.min; P less than 0.005) and late (10-180 min: 4,582 +/- 689 vs. 8,895 +/- 1,316 microU.ml-1.min; P less than 0.005) insulin secretory phases. These data demonstrate that 1) the improved insulin action in healthy trained subjects is due to increased sensitivity to insulin, with no change in responsiveness to insulin, and 2) trained subjects have a smaller plasma insulin response to an identical glucose stimulus than untrained individuals.

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