Effects of sugar‐sweetened beverages on plasma acylation stimulating protein, leptin and adiponectin: Relationships with Metabolic Outcomes

Rezvani, Reza; Cianflone, Katherine; McGahan, John P.; Berglund, Lars; Bremer, Andrew A.; Keim, Nancy L.; Griffen, Steven C.; Havel, Peter J.; Stanhope, Kimber L.

doi:10.1002/oby.20437

Cited by 38 publications

(49 citation statements)

References 42 publications

(48 reference statements)

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“…Previous studies have shown that excess sugar consumption is sufficient to decrease serum adiponectin levels in rats [50] and humans [51]. In the present study, we observed that serum adiponectin levels were decreased in mice fed diets containing high sugar.…”

Section: Discussionsupporting

confidence: 71%

Dietary effects on liver tumor burden in mice treated with the hepatocellular carcinogen diethylnitrosamine

Healy¹,

Chow²,

Byrne³

et al. 2015

Journal of Hepatology

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Background & Aims Mice exposed to the hepatocellular carcinogen diethylnitrosamine at 2 weeks of age have a high risk of developing primary liver tumors later in life. Previous studies have demonstrated that diethylnitrosamine-treated mice have increased tumor burden when fed an obesigenic “Western” diet rich in lard fat and sugar. However, the role of dietary fats versus sugars in the promotion of liver cancer is poorly understood. The aim of this study was to determine how altering dietary fats versus sugars affects tumor burden in the diethylnitrosamine model. Methods C57BL/6N mice were treated with diethylnitrosamine at 2 weeks of age and, from 6 to 32 weeks of age, fed one of five diets that differed in fat and sugar content including normal chow, ketogenic, and Western diets. Results Mice fed sugar-rich diets had the greatest tumor burden irrespective of dietary fat content. In contrast, mice fed a high-fat low-sugar diet had the least tumor burden despite obesity and glucose intolerance. When evaluated as independent variables, tumor burden was positively correlated with hepatic fat accumulation, postprandial insulin, and liver IL-6, and inversely correlated with serum adiponectin. In contrast, tumor burden did not correlate with adiposity, fasting insulin, or glucose intolerance. Furthermore, mice fed high sugar diets had lower liver expression of p21 and cleaved caspase-3 compared to mice fed low sugar diets. Conclusions These data indicate that dietary sugar intake contributes to liver tumor burden independent of excess adiposity or insulin resistance in mice treated with diethylnitrosamine.

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Section: Discussionsupporting

confidence: 71%

Dietary effects on liver tumor burden in mice treated with the hepatocellular carcinogen diethylnitrosamine

Healy¹,

Chow²,

Byrne³

et al. 2015

Journal of Hepatology

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“…Food intake appeared to be similar and weight gain was comparable between the subjects consuming 25% Ereq as fructose- or glucose-sweetened beverages with ad libitum diets for 8 weeks (33). However, in these same subjects, we also observed a fructose-induced decrease in 24-h leptin levels (123), and a decrease in fasting energy expenditure that was not observed with glucose consumption (31). Why then did the subjects consuming fructose fail to show increased body weight gain compared with the subjects consuming glucose?…”

Section: Introductionmentioning

confidence: 54%

“…Leptin production by adipocytes is regulated by insulin-mediated glucose metabolism (121). Ingestion of fructose does not result in meal-related increases of plasma glucose or insulin concentrations, therefore both short (34, 122) and long-term (123) studies demonstrate that meals accompanied with fructose-sweetened beverages result in reduced circulating leptin concentrations compared with glucose-sweetened beverages. Leptin acts, along with insulin, in the hypothalamus to regulate food intake and energy metabolism via neuropeptide systems including neuropeptide-Y and melanocortins.…”

Section: Introductionmentioning

confidence: 99%

Sugar consumption, metabolic disease and obesity: The state of the controversy

Stanhope

2015

Critical Reviews in Clinical Laboratory Sciences

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577

390

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The impact of sugar consumption on health continues to be a controversial topic. The objective of this review is to discuss the evidence and lack of evidence that allows the controversy to continue, and why resolution of the controversy is important. There are plausible mechanisms and research evidence that support the suggestion that consumption of excess sugar promotes the development of cardiovascular disease (CVD) and type 2 diabetes (T2DM) both directly and indirectly. The direct pathway involves the unregulated hepatic uptake and metabolism of fructose, which leads to liver lipid accumulation, dyslipidemia, decreased insulin sensitivity and increased uric acid levels. The epidemiological data suggest that these direct effects of fructose are pertinent to the consumption of the fructose-containing sugars, sucrose and HFCS, which are the predominant added sugars. Consumption of added sugar is associated with development and/or prevalence of fatty liver, dyslipidemia, insulin resistance, hyperuricemia, cardiovascular disease and type 2 diabetes, and many of these associations are independent of body weight gain or total energy intake. There are diet intervention studies in which human subjects exhibited increased circulating lipids and decreased insulin sensitivity when consuming high sugar compared with control diets. Most recently, our group has reported that supplementing the ad libitum diets of young adults with beverages containing 0, 10, 17.5 or 25% of daily energy requirement (Ereq) as high fructose corn syrup (HFCS) increased lipid/lipoprotein risk factors for cardiovascular disease (CVD) and uric acid in a dose response manner. However, un-confounded studies conducted in healthy humans under a controlled, energy-balanced diet protocol that allow determination of the effects of sugar with diets that do not allow for body weight gain are lacking. Furthermore, there are recent reports that conclude that there are no adverse effects of consuming beverages containing up to 30% Ereq sucrose or HFCS, and the conclusions from several meta-analyses suggest that fructose has no specific adverse effects relative to any other carbohydrate. Consumption of excess sugar may also promote the development the development of CVD and T2DM indirectly by causing increased body weight and fat gain, but this is also a topic of controversy. Mechanistically, it is plausible that fructose consumption causes increased energy intake and reduced energy expenditure due to its failure to stimulate leptin production. Functional magnetic resonance imaging of the brain demonstrates that the brain responds differently to fructose or fructose-containing sugars compared with glucose or aspartame. There are epidemiological studies which show sugar consumption is associated with body weight gain, and there are intervention studies in which consumption of ad libitum high sugar diets promoted increased body weight gain compared with consumption of ad libitum low sugar diets. However, there are no studies in which energy intake and weight gai...

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“…Decreased adiponectin levels in systemic circulation closely correlates with accumulation of vesical adipose and dysregulation of insulin-stimulated glucose uptake and utilization [154]. Therefore, abdominal and visceral adiposity, reduced insulin-sensitive visceral adipocytes, as well as increased body weight and fat under high fructose feeding [29,155], cause adiponectin secretion reduction [151].…”

Section: Adiponectinmentioning

confidence: 99%

Dietary Fructose and Glucose: The Multifacetted Aspects of Their Metabolism and Implication for Human Health

2018

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Effects of sugar‐sweetened beverages on plasma acylation stimulating protein, leptin and adiponectin: Relationships with Metabolic Outcomes

Cited by 38 publications

References 42 publications

Dietary effects on liver tumor burden in mice treated with the hepatocellular carcinogen diethylnitrosamine

Dietary effects on liver tumor burden in mice treated with the hepatocellular carcinogen diethylnitrosamine

Sugar consumption, metabolic disease and obesity: The state of the controversy

Dietary Fructose and Glucose: The Multifacetted Aspects of Their Metabolism and Implication for Human Health

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