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Genome-wide association studies have identified thousands of variants that are associated with numerous phenotypes. One such variant, rs13266634, a nonsynonymous single nucleotide polymorphism in the solute carrier family 30 (zinc transporter) member eight gene, is associated with a 53% increase in the risk of developing type 2 diabetes (T2D). We hypothesized that individuals with the protective allele against T2D would show a positive response to short-term and long-term resistance exercise. Two cohorts of young adults--the Eccentric Muscle Damage (EMD; n = 156) cohort and the Functional Single Nucleotide Polymorphisms Associated with Muscle Size and Strength Study (FAMuSS; n = 874)--were tested for association of the rs13266634 variant with measures of skeletal muscle response to resistance exercise. Our results were sexually dimorphic in both cohorts. Men in the EMD study with two copies of the protective allele showed less post-exercise bout strength loss, less soreness, and lower creatine kinase values. In addition, men in the FAMuSS, homozygous for the protective allele, showed higher pre-exercise strength and larger arm skeletal muscle volume, but did not show a significant difference in skeletal muscle hypertrophy or strength with resistance training. Diabetes 2014;63:363-368 | DOI: 10.2337/db13-1150, Genome-wide association studies (GWASs) are extensively used as a tool to discover common single nucleotide polymorphisms (SNPs) associated with complex disease phenotypes such as type 2 diabetes (T2D), dyslipidemia, and [...]

High-fructose corn syrup (HFCS) has been implicated in excess weight gain through mechanisms seen in some acute feeding studies and by virtue of its abundance in the food supply during years of increasing obesity. Compared with pure glucose, fructose is thought to be associated with insufficient secretion of insulin and leptin and suppression of ghrelin. However, when HFCS is compared with sucrose, the more commonly consumed sweetener, such differences are not apparent, and appetite and energy intake do not differ in the short-term. Longer-term studies on connections between HFCS, potential mechanisms, and body weight have not been conducted. The main objective of this review was to examine collective data on associations between consumption of HFCS and energy balance, with particular focus on energy intake and its regulation.

Background: Recent reports suggest that dietary energy density (ED) is associated with diet quality, energy intake, and body weight. Breakfast consumption was also associated with diet quality and body weight; however, little is known about the association of breakfast consumption with dietary ED. Objectives: We examined differences in the ED (in energy content/g of food) of diets between breakfast consumers and nonconsumers, and in breakfast reporters we examined the association of ED of breakfast foods with ED of nonbreakfast foods, diet quality, and body mass index (BMI; in kg/[m.sup.2]). Design: We combined dietary data from the 3 continuous National Health and Nutrition Examination Surveys (1999-2004) to determine the ED (in kcal/g) of foods and nutritive beverages and the ED of foods only (n = 12 316; [greater than or equal to] 20 y). Linear and logistic regression methods were used to examine the independent associations of breakfast reporting or breakfast ED with 24-h ED, nonbreakfast ED, diet quality, and BMI. Results: The ED of 24-h dietary intake was lower among breakfast reporters than among nonreporters. Women breakfast reporters (but not men) had lower BMI than did nonreporters (27.9 [+ or -] 0.2 compared with 29.4 [+ or -] 0.4; P = 0.001). With increasing breakfast ED, nonbreakfast ED and fat intake increased, but micronutrient intake and the likelihood of mention of all 5 food groups declined. BMI increased with increasing breakfast ED in men but with increasing nonbreakfast ED in women (P [less than or equal to] 0.001). Conclusions: Our results support recommendations to encourage breakfast consumption and suggest that the ED of breakfast was associated with diet quality, overall diet ED, and body weight.

Study was conducted to examine associations among the angiotensin I-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism and the response to a 12-wk unilateral, upper-arm resistance training (RT) program in the trained and untrained arms. It was found that the ACE ID genotype associated with the contralateral muscle strength and size effects of unilateral RT.

Several modular studies are conducted to determine the impact of resistance training on the vascular remodeling of the upper arm in humans. The discussed vascular remodeling is shown to lead to an increase in the brachial artery diameter of the arm.

Associations among myostatin (MSTN) 2379 A > G and 163 G > A and follistatin (FST) -5003 A > T and -833 G > T single nucleotide polymorphisms on muscle size and strength response to resistance training are studied. MSTN 2379 A > G and FST -5003 A > T were associated with associated with baseline muscle size and strength among African Americans.

Resistance training and an exercise program did not necessarily reduce sub-cutaneous fat in either of the sexes. The results of this study are presented.

Allometric scaling based on the theory that all humans have the same shape but differ only in size, has been used to develop scaling models of isometric biceps muscle strength and test the appropriateness using regression diagnostics. Results concluded that these exponents are appropriate for scaling isometric biceps strength in adult males.

A study assessed variability in muscle size and strength changes in a large cohort of men and women after a unilateral resistance-training program in the elbow flexors. It is concluded that men had only a slight advantage in relative size gains compared with women, whereas women outpaced men in relative gains in strength.

The consumption of sugar and its relation to various potential adverse health consequences are the subjects of considerable debate and controversy. This supplement to Advances in Nutritionprovides an expanded summary of a symposium held on 26 April 2014 entitled “Sugars and Health Controversies: What Does the Science Say?” as part of the ASN Scientific Sessions and Annual Meeting at Experimental Biology 2014. The articles in the supplement discuss results of current systematic reviews and meta-analyses as well as randomized controlled trials and draw implications for public policy considerations. In addition, future research gaps are identified. Current research trials conducted with commonly consumed sugars [e.g., sucrose and high-fructose corn syrup (HFCS)] do not support a unique relation to obesity, metabolic syndrome, diabetes, risk factors for heart disease, or nonalcoholic fatty liver disease. Neurologic differences in response to studies that used pure fructose compared with pure glucose have not been confirmed using typical sugars that are consumed (i.e., sucrose and HFCS), which contain ∼50% glucose and fructose. We conclude that added sugars consumed in the normal forms in which humans consume them, at amounts typical of the human diet and for the time period studied in randomized controlled trials, do not result in adverse health consequences. Although more research trials are needed in many areas of sugar consumption and health, there is little scientific justification for recommending restricting sugar consumption below the reasonable upper limit recommended by the Dietary Guidelines for Americans, 2010 of no more than 25% of calories.

Cardiovascular disease (CVD) is the single largest cause of mortality in the United States and worldwide. Numerous risk factors have been identified for CVD, including a number of nutritional factors. Recently, attention has been focused on fructose-containing sugars and their putative link to risk factors for CVD. In this review, we focus on recent studies related to sugar consumption and cardiovascular risk factors including lipids, blood pressure, obesity, insulin resistance, diabetes, and the metabolic syndrome. We then examine the scientific basis for competing recommendations for sugar intake. We conclude that although it appears prudent to avoid excessive consumption of fructosecontaining sugars, levels within the normal range of human consumption are not uniquely related to CVD risk factors with the exception of triglycerides, which may rise when simple sugars exceed 20% of energy per day, particularly in hypercaloric settings.

Both controversy and confusion exist concerning fructose, sucrose, and high-fructose corn syrup (HFCS) with respect to their metabolism and health effects. These concerns have often been fueled by speculation based on limited data or animal studies. In retrospect, recent controversies arose when a scientific commentary was published suggesting a possible unique link between HFCS consumption and obesity. Since then, a broad scientific consensus has emerged that there are no metabolic or endocrine response differences between HFCS and sucrose related to obesity or any other adverse health outcome. This equivalence is not surprising given that both of these sugars contain approximately equal amounts of fructose and glucose, contain the same number of calories, possess the same level of sweetness, and are absorbed identically through the gastrointestinal tract. Research comparing pure fructose with pure glucose, although interesting from a scientific point of view, has limited application to human nutrition given that neither is consumed to an appreciable degree in isolation in the human diet. Whether there is a link between fructose, HFCS, or sucrose and increased risk of heart disease, metabolic syndrome, or fatty infiltration of the liver or muscle remains in dispute with different studies using different methodologies arriving at different conclusions. Further randomized clinical trials are needed to resolve many of these issues. The purpose of this review is to summarize current knowledge about the metabolism, endocrine responses, and potential health effects of sucrose, HFCS, and fructose.

Genome-wide association studies (GWASs) have identified polymorphic loci associated with coronary artery disease (CAD) risk factors (i.e. serum lipids) in adult populations (42–69 y). We hypothesized that younger populations would show a greater relative genetic component due to fewer confounding variables. We examined the influence of 20 GWAS loci associated with serum lipids and insulin metabolism, in a university student cohort (n = 548; mean age = 24 y), and replicated statistically associated results in a second study cohort of primary school students (n = 810, mean age = 11.5 y). Nineteen loci showed no relationship with studied risk factors in young adults. However, the ancestral allele of the rs646776 (SORT1) locus was strongly associated with increased LDL (C) in young adults [TT: 97.6 ± 1.0 mg/dL (n = 345) versus CT/CC: 87.3 ± 1.0 mg/dL (n = 203); p = 3 × 10×6] and children [TT: 94.0 ± 1.3 mg/dL (n = 551) versus CT/CC: 84.7 ± 1.4 mg/dL (n = 259); p = 4 × 10×6]. This locus is responsible for 3.6% of population variance in young adults and 2.5% of population variance in children. The effect size of the SORT1 locus is considerably higher in young populations (2.5–4.1%) compared with older subjects (1%).

To determine the effect of endogenous opioids on catecholamine response during intense exercise [80% maximal oxygen uptake ( $$\dot V$$ O2max)], nine fit men [mean (SE) ( $$\dot V$$ O2max, 63.9 (1.7) ml · kg-1 · min-1; age 27.6 (1.6) years] were studied during two treadmill exercise trials. A double-blind experimental design was used with subjects undertaking the two exercise trials in counterbalanced order. Exercise trials were 20 min in duration and were conducted 7 days apart. One exercise trial was undertaken following administration of naloxone (N; 1.2 mmol · l-1; 3 ml) and the other after receiving a placebo (P; 0.9% saline; 3 ml). Prior to each experimental trial a flexible catheter was placed into an antecubital vein and baseline blood samples were collected. Immediately afterwards, each subject received bolus injection of either N or P. Blood samples were also collected after 20 min of continuous exercise while running. Epinephrine and norepinephrine were higher (P < 0.05) in the N than P exercise trial with mean (SE) values of 1679 (196) versus 1196 (155) pmol · l-1 and 24 (2.2) versus 20 (1.7) nmol · · l-1 respectively. Glucose and lactate were higher (P < 0.05) in the N than P exercise trial with values of 7 (0.37) versus 5.9 (0.31) mmol · l-1 and 6.9 (1.1) versus 5.3 (0.9) mmol · l-1 respectively. These data suggest an opioid inhibition in the release of catecholamines during intense exercise.

We characterized the effect of ten days of training on lipid metabolism in 6 [age 37.2 (2.3) years] sedentary, obese [BMI 34.4?(3.0)?kg?·?m -2] males with normal glucose tolerance. An oral glucose tolerance test was performed prior to and at the end of the 10?d of training period. The duration of each daily exercise session was 40?min at an intensity equivalent to ˜75% of the age predicted maximum heart rate. Blood measurements were performed after an overnight fast, before and at the end of the 10?d period. Plasma triacylglycerol was significantly ( p?-1). Very low density lipoprotein-triacylglycerol was also significantly?( p?-1). No significant changes in high density lipoprotein-cholesterol were observed as a result of training. Following training fasting plasma glucose and fasting plasma insulin were significantly reduced [Glucose: 5.9 (0.2)?mmol?·?l -1 vs.?5.3 (0.22)?mmol?·?l -1 ( p?-1 vs. 200.9 (30.1) ??·?mol?·?l -1, p?=?0.05]. The total area under the glucose curve during the OGTT decreased significantly ( p?

ß-Endorphin (BE) infusion at rest can influence insulin and glucagon levels and thus may affect glucose availability during exercise. To clarify the effect of BE on levels of insulin, glucagon and glucose during exercise, 72 untrained male Sprague-Dawley rats were infused i.v. with either: (1) BE (bolus 0.05?mg?·?kg -1 +0.05?mg?·?kg -1?·?h -1, n?=?24); (2) naloxone (N, bolus 0.8?mg?·?kg -1?+?0.4?mg?·?kg -1, n?=?24); or (3) volume-matched saline (S, n?=?24). Six rats from each group were killed after 0, 60, 90 or 120 min of running at 22?m?·?min -1, at 0% gradient. BE infusion resulted in higher plasma glucose levels at 60?min [5.93 (0.32)?mM] and 90?min [4.16 (0.29)?mM] of exercise compared to S [4.62 (0.27) and 3.41 (0.26?mM] and N [4.97 (0.38) and 3.44 (0.25)?mM]. Insulin levels decreased to a greater extent with BE [21.5 (0.9) and 18.3 (0.6) uIU?·?ml -1] at 60 and 90?min compared to S [24.5 (0.5) and 20.6 (0.6)?uIU?·?ml -1] and N [24.5 (0.4) and 21.6 (0.7)?uIU?· ml -1] groups. Plasma C-peptide declined to a greater extent at 60 and 90?min of exercise with BE infusion compared to both S and N. BE infusion increased glucagon at all times during exercise compared to S and N. These data suggest that BE infusion during exercise influences plasma glucose by augmenting glucagon levels and attenuating insulin release.

Eight fit men [maximum oxygen consumption ( O 2max) 64.6 (1.9) ml?·?kg -1?·?min -1, aged 28.3 (1.7) years (SE in parentheses) were studied during two treadmill exercise trials to determine the effect of endogenous opioids on insulin and glucagon immunoreactivity during intense exercise (80% O 2max). A double-blind experimental design was used with subjects undertaking the two exercise trials in counterbalanced order. Exercise trials were 20 min in duration and were conducted 7 days apart. One exercise trial was undertaken following administration of naloxone (N; 1.2 mg; 3?ml) and the other after receiving a placebo (P; 0.9% NaCl saline; 3?ml). Prior to each experimental trial a flexible catheter was placed into an antecubital vein and baseline blood samples were collected. Immediately after, each subject received either a N or P bolus injection. Blood samples were also collected after 20?min of continuous exercise (running). Glucagon was higher ( P?-1 vs 127.2 (7.6) ng?·?l -1]. There were no differences in insulin during exercise between the P and N trials [50.2 (4.3) pmol?·?l -1 vs 43.8 (5) pmol?·?l -1]. These data suggest that endogenous opioids may augment the glucagon response during intense exercise.