Excessive fruit consumption during the second trimester is associated with increased likelihood of gestational diabetes mellitus: a prospective study

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Abstract

This study aimed to investigate the association between fruit consumption during the second trimester and the occurrence of gestational diabetes mellitus (GDM). A prospective study with 772 female participants was conducted in China from April 2013 to August 2014. Dietary intake was assessed in face-to-face and telephone interviews using a 3-day food record. GDM was ascertained using a standard 75 g 2 hour oral glucose tolerance test. Multivariable logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) after adjustment for various confounders. Of the 772 participants, 169 were diagnosed with GDM during the period under study. Greater total fruit consumption during the second trimester was associated with a higher likelihood of GDM (highest vs. lowest quartile: adjusted OR4.82, 95% CI 2.38 to 9.76). Fruits with a moderate or high glycaemic index (GI) were positively associated with the occurrence of GDM. Fruit subgroups were also categorised by polyphenol content, and tropical-fruit and citrus-fruit consumption was found to be positively related to the occurrence of GDM. These findings suggest that the excessive consumption of fruit, especially fruit with moderate or high GI values, tropical-fruit and citrus-fruit, increases the likelihood of GDM.

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Most cited references 30

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Richard J. Johnson, Mark Segal, Yuri Sautin … (2007)

Currently, we are experiencing an epidemic of cardiorenal disease characterized by increasing rates of obesity, hypertension, the metabolic syndrome, type 2 diabetes, and kidney disease. Whereas excessive caloric intake and physical inactivity are likely important factors driving the obesity epidemic, it is important to consider additional mechanisms. We revisit an old hypothesis that sugar, particularly excessive fructose intake, has a critical role in the epidemic of cardiorenal disease. We also present evidence that the unique ability of fructose to induce an increase in uric acid may be a major mechanism by which fructose can cause cardiorenal disease. Finally, we suggest that high intakes of fructose in African Americans may explain their greater predisposition to develop cardiorenal disease, and we provide a list of testable predictions to evaluate this hypothesis.

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Fructose, weight gain, and the insulin resistance syndrome.

Sharon S Elliott, Nancy Keim, Judith Stern … (2002)

This review explores whether fructose consumption might be a contributing factor to the development of obesity and the accompanying metabolic abnormalities observed in the insulin resistance syndrome. The per capita disappearance data for fructose from the combined consumption of sucrose and high-fructose corn syrup have increased by 26%, from 64 g/d in 1970 to 81 g/d in 1997. Both plasma insulin and leptin act in the central nervous system in the long-term regulation of energy homeostasis. Because fructose does not stimulate insulin secretion from pancreatic beta cells, the consumption of foods and beverages containing fructose produces smaller postprandial insulin excursions than does consumption of glucose-containing carbohydrate. Because leptin production is regulated by insulin responses to meals, fructose consumption also reduces circulating leptin concentrations. The combined effects of lowered circulating leptin and insulin in individuals who consume diets that are high in dietary fructose could therefore increase the likelihood of weight gain and its associated metabolic sequelae. In addition, fructose, compared with glucose, is preferentially metabolized to lipid in the liver. Fructose consumption induces insulin resistance, impaired glucose tolerance, hyperinsulinemia, hypertriacylglycerolemia, and hypertension in animal models. The data in humans are less clear. Although there are existing data on the metabolic and endocrine effects of dietary fructose that suggest that increased consumption of fructose may be detrimental in terms of body weight and adiposity and the metabolic indexes associated with the insulin resistance syndrome, much more research is needed to fully understand the metabolic effect of dietary fructose in humans.