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1.  Twenty-four Hour Endocrine and Metabolic Profiles Following Consumption of High Fructose Corn Syrup-, Sucrose- Fructose-, and Glucose-Sweetened Beverages with Meals 
Background
We have reported that compared with glucose-sweetened beverages, consuming fructose-sweetened beverages with meals results in lower 24-h circulating glucose, insulin and leptin concentrations, and elevated triacylglycerol (TG). However, pure fructose and glucose are not commonly used as sweeteners. High fructose corn syrup (HFCS) has replaced sucrose as the predominant sweetener in beverages in the U.S.
Objective
We compared the metabolic/endocrine effects of HFCS with sucrose, and in a subset of subjects with pure fructose and glucose.
Design
34 men and women consumed 3 isocaloric meals with either sucrose- or HFCS-sweetened beverages, and blood samples were collected over 24 hours. Eight of the male subjects were also studied when fructose- or glucose-sweetened beverages were consumed.
Results
In 34 subjects, 24-h glucose, insulin, leptin, ghrelin and TG profiles were similar between days that sucrose or HFCS were consumed. Postprandial TG excursions after HFCS or sucrose were larger in men than women. In the men in whom the effects of 4 sweeteners were compared, the 24-h glucose and insulin responses induced by HFCS and sucrose were intermediate between the lower responses during consumption of fructose and the higher responses during glucose. Unexpectedly, postprandial TG profiles after HFCS or sucrose were not intermediate, but comparably high as after pure fructose.
Conclusions
Sucrose and HFCS do not have substantially different short-term endocrine/metabolic effects. In male subjects, short-term consumption of sucrose and HFCS resulted in postprandial TG responses comparable to those induced by fructose.
PMCID: PMC3037416  PMID: 18469239
glucose; fructose; high fructose corn syrup; sucrose; insulin; leptin; ghrelin; triacylglycerol; free fatty acids; postprandial hypertriacylglycerolemia; humans
2.  Consumption of fructose-sweetened beverages for 10 weeks increases postprandial triacylglycerol and apolipoprotein-B concentrations in overweight and obese women 
The British journal of nutrition  2008;100(5):947-952.
Fructose consumption in the USA has increased over the past three decades. During this time, obesity, insulin resistance and the metabolic syndrome have also increased in prevalence. While diets high in fructose have been shown to promote insulin resistance and increase TAG concentrations in animals, there are insufficient data available regarding the long-term metabolic effects of fructose consumption in humans. The objective of the present study was to investigate the metabolic effects of 10-week consumption of fructose-sweetened beverages in human subjects under energy-balanced conditions in a controlled research setting. Following a 4-week weight-maintaining complex carbohydrate diet, seven overweight or obese (BMI 26.8–33.3 kg/m2) postmenopausal women were fed an isoenergetic intervention diet, which included a fructose-sweetened beverage with each meal, for 10 weeks. The intervention diet provided 15% of energy from protein, 30% from fat and 55% from carbohydrate (30% complex carbohydrate, 25% fructose). Fasting and postprandial glucose, insulin, TAG and apoB concentrations were measured. Fructose consumption increased fasting glucose concentrations and decreased meal-associated glucose and insulin responses (P=0.0002, P=0.007 and P=0.013, respectively). Moreover, after 10 weeks of fructose consumption, 14 h postprandial TAG profiles were significantly increased, with the area under the curve at 10 weeks being 141% higher than at baseline (P=0.04). Fructose also increased fasting apoB concentrations by 19% (P=0.043 v. baseline). In summary, consumption of fructose-sweetened beverages increased postprandial TAG and fasting apoB concentrations, and the present results suggest that long-term consumption of diets high in fructose could lead to an increased risk of CVD.
doi:10.1017/S0007114508968252
PMCID: PMC3038917  PMID: 18384705
Fructose; Glucose; Insulin; Hypertriacylglycerolaemia; Apolipoprotein-B
3.  Association of Adiponectin and Mortality in Older Adults: Health ABC Study 
Diabetologia  2009;52(4):591-595.
Background
Despite the widely reported inverse associations with insulin resistance and adiposity, adiponectin has been associated with both increased and decreased risk of cardiovascular disease. We examined whether adiponectin is associated with total and cardiovascular mortality in a large population of older adults.
Methods
We analyzed data from 3,075 well-functioning adults ages 69–79 years. Total adiponectin concentrations were measured at baseline and body composition was measured with abdominal and thigh CT scans. Mortality data was obtained over 6.6±1.6 years. We used Cox proportional hazards models adjusting for covariates in stages to examine the association between adiponectin and total and cardiovascular mortality.
Results
There were 679 deaths and 38% were from cardiovascular disease. Unadjusted levels of adiponectin were not associated with total or cardiovascular mortality. However, after adjusting for sex and race, adiponectin was associated with an increased risk of both total (HR 1.26, 95% CI 1.15–1.37, per SD) and cardiovascular mortality (HR 1.35, 95% CI 1.17–1.56, per SD). Further adjustment for study site, smoking, hypertension, diabetes, prevalent heart disease, HDL, LDL, cystatin C, fasting insulin, triglycerides, BMI, visceral fat, thigh intermuscular fat, and thigh muscle area did not attenuate this association. This association between adiponectin and increased mortality risk did not vary by sex, race, BMI, diabetes, smoking, or weight loss.
Conclusions
Higher levels of adiponectin were associated with increased risk of total and cardiovascular mortality in this study of well-functioning community-dwelling older persons. This paradoxical association needs further study of underlying factors that might explain these results including differential association for high molecular weight adiponectin.
doi:10.1007/s00125-009-1261-7
PMCID: PMC2756826  PMID: 19159917
4.  Physiological, Pharmacological, and Nutritional Regulation of Circulating Adiponectin Concentrations in Humans 
Abstract
Adiponectin is an adipocyte hormone that links visceral adiposity with insulin resistance and atherosclerosis. It is unique among adipocyte-derived hormones in that its circulating concentrations are inversely proportional to adiposity, and low adiponectin concentrations predict the development of type 2 diabetes and cardiovascular disease. Consequently, in the decade since its discovery, adiponectin has generated immense interest as a potential therapeutic target for the metabolic syndrome and diabetes.
This review summarizes current research regarding the regulation of circulating adiponectin concentrations by physiological, pharmacological, and nutritional factors, with an emphasis on human studies. In humans, plasma adiponectin concentrations are influenced by age and gender, and are inversely proportional to visceral adiposity. In vitro studies suggest that adiponectin production may be determined primarily by adipocyte size and insulin sensitivity, with larger, insulin-resistant adipocytes producing less adiponectin. While adiponectin concentrations are unchanged after meal ingestion, they are increased by significant weight loss, such as after bariatric surgery. In addition, adiponectin production is inhibited by a number of hormones, including testosterone, prolactin, glucocorticoids and growth hormone, and by inflammation and oxidative stress in adipose tissue. Smoking decreases, while moderate alcohol consumption increases, circulating adiponectin concentrations. Dietary fatty acid composition in rodents influences adiponectin production via ligand-activated nuclear receptors (PPARs); however, current evidence in humans is equivocal. In addition to PPAR agonists (such as thiazolidinediones and fibrates), a number of pharmacological agents (angiotensin receptor type 1 blockers, ACE inhibitors, and cannabinoid receptor antagonists) used in treatment of the metabolic syndrome also increase adiponectin concentrations in humans.
doi:10.1089/met.2007.0029
PMCID: PMC3190268  PMID: 18510434
5.  CRP and Adiponectin and Its Oligomers in the Metabolic Syndrome 
The metabolic syndrome (MetS) confers an increased risk for diabetes and cardiovascular disease. Although high-sensitive C-reactive protein (hsCRP) concentrations are higher and adiponectin concentrations lower in MetS, there is no reliable biochemical measure that can capture its various features. We evaluated whether hsCRP, adiponectin, or the ratio of adiponectin or its oligomers, especially the high-molecular-weight (HMW) oligomer, to hsCRP predict MetS in 123 subjects with MetS compared with that in 91 healthy control subjects. MetS subjects had significantly higher hsCRP levels and lower total adiponectin and oligomer levels relative to control subjects (P < .0001). The HMW/total adiponectin and adiponectin/CRP ratios were significantly lower in MetS subjects than control subjects (P < .005). The odds ratio (OR) of MetS using the 75th percentile cutoff for CRP was 3.8 (95% confidence interval [CI], 2.1–6.8) and equivalent to low total adiponectin (OR, 2.5; 95% CI, 1.3–4.5), its oligomers, or the adiponectin/hsCRP ratio (OR, 2.6; 95% CI, 1.5, 4.8). Thus, measurements of CRP, adiponectin, or its oligomers provide robust biomarkers for predicting MetS.
doi:10.1309/RN84K51B2JJY1Y0B
PMCID: PMC2664630  PMID: 18426744
C-reactive protein; Adiponectin; Biomarker; Metabolic syndrome
6.  Effect of dietary n–3 polyunsaturated fatty acids on plasma total and high-molecular-weight adiponectin concentrations in overweight to moderately obese men and women123 
Background
Recent studies indicated that dietary n–3 polyunsaturated fatty acids (PUFAs) increase circulating adiponectin concentrations in rodents.
Objective
We aimed to investigate whether a diet rich in n–3 PUFAs increased plasma concentrations of total or high-molecular-weight (HMW) adiponectin in healthy overweight-to-moderately obese men and women.
Design
Sixteen women and 10 men with a body mass index (in kg/m2) between 28 and 33 were randomly assigned to consume a diet rich in n–3 PUFAs (3.5% of energy intake) from both plant and marine sources or a control diet (0.5% of energy intake from n–3 PUFAs). For the first 2 wk, these diets were consumed under isocaloric conditions; then followed a 12-wk period of ad libitum consumption that was associated with a moderate loss of ≈3.5% of body weight in both groups. Total and HMW adiponectin plasma concentrations were measured before and after each diet phase.
Results
Plasma fasting adiponectin concentrations did not change during the isocaloric period, but they increased modestly (≈10%) during the ad libitum period when subjects lost weight [P = 0.009 for time in repeated-measures analysis of variance] and to a similar extent in subjects consuming the control (x̄ ± SD: 0.42 ± 0.69 μg/mL) and n–3 PUFA (0.45 ± 0.85 μg/mL) diets (P = 0.920 for time × treatment interaction). Plasma concentrations of HMW adiponectin did not change significantly during the study.
Conclusion
Dietary n–3 PUFAs consumed at levels of 3.5% of energy intake do not significantly increase plasma or HMW adiponectin concentrations in overweight-to-moderately obese healthy men and women over the course of 14 wk.
PMCID: PMC2265085  PMID: 18258624
Adiponectin; fatty acids; omega-3; n-3; diet; obesity; overweight; humans
7.  Lack of Support for the Association between GAD2 Polymorphisms and Severe Human Obesity 
PLoS Biology  2005;3(9):e315.
The demonstration of association between common genetic variants and chronic human diseases such as obesity could have profound implications for the prediction, prevention, and treatment of these conditions. Unequivocal proof of such an association, however, requires independent replication of initial positive findings. Recently, three (−243 A>G, +61450 C>A, and +83897 T>A) single nucleotide polymorphisms (SNPs) within glutamate decarboxylase 2 (GAD2) were found to be associated with class III obesity (body mass index > 40 kg/m2). The association was observed among 188 families (612 individuals) segregating the condition, and a case-control study of 575 cases and 646 lean controls. Functional data supporting a pathophysiological role for one of the SNPs (−243 A>G) were also presented. The gene GAD2 encodes the 65-kDa subunit of glutamic acid decarboxylase—GAD65. In the present study, we attempted to replicate this association in larger groups of individuals, and to extend the functional studies of the −243 A>G SNP. Among 2,359 individuals comprising 693 German nuclear families with severe, early-onset obesity, we found no evidence for a relationship between the three GAD2 SNPs and obesity, whether SNPs were studied individually or as haplotypes. In two independent case-control studies (a total of 680 class III obesity cases and 1,186 lean controls), there was no significant relationship between the −243 A>G SNP and obesity (OR = 0.99, 95% CI 0.83–1.18, p = 0.89) in the pooled sample. These negative findings were recapitulated in a meta-analysis, incorporating all published data for the association between the −243G allele and class III obesity, which yielded an OR of 1.11 (95% CI 0.90–1.36, p = 0.28) in a total sample of 1,252 class III obese cases and 1,800 lean controls. Moreover, analysis of common haplotypes encompassing the GAD2 locus revealed no association with severe obesity in families with the condition. We also obtained functional data for the −243 A>G SNP that does not support a pathophysiological role for this variant in obesity. Potential confounding variables in association studies involving common variants and complex diseases (low power to detect modest genetic effects, overinterpretation of marginal data, population stratification, and biological plausibility) are also discussed in the context of GAD2 and severe obesity.
A large genetic study involving multiple populations is not able to replicate previous findings linking variation in the GAD2 gene to susceptibility to obesity.
doi:10.1371/journal.pbio.0030315
PMCID: PMC1193520  PMID: 16122350

Results 1-7 (7)