Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women.

By K. Teff, Sharon S Elliott, Matthias Tschöp, T. Kieffer, Daniel J. Rader, M. Heiman, R. Townsend, N. Keim, D. D’Alessio, P. Havel. Journal of Clinical Endocrinology and Metabolism, 2004

753 citations recorded by the source corpus.

Subfields: Endocrine and Autonomic Systems, Endocrinology, Diabetes and Metabolism, Physiology

View Paper: https://www.semanticscholar.org/paper/b1c307beb677bf4718b3ba243c92dfbf09a361b7

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Endocrine and Autonomic Systems

1. P. Havel
2. K. Stanhope

In Endocrinology, Diabetes and Metabolism

1. K. Stanhope
2. P. Havel
3. Richard J. Johnson
4. Ronald M. Krauss
5. F. B. Hu

In Physiology

1. P. Havel
2. K. Stanhope
3. Richard J. Johnson
4. N. Keim
5. T. Nakagawa
6. Y. Sautin
7. Ronald M. Krauss

Citations in the corpus

• Nonalcoholic fatty liver disease: pathology and pathogenesis. (2010, background): “For reasons that are not well understood, fructose (but not glucose) fails to stimulate postprandial ghrelin or insulin secretion, thus failing to initiate the central satiety response (77).”
• Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. (2005, methodology): “In a recently published study, the short-term effects of consuming fructose- and glucose-sweetened beverages (providing 30% of total energy) consumed with three meals over a 24-hour period were compared in 12 normal-weight young women with normal fasting triglyceride levels.(22) In this crossover st”
• Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. (2009, background): “Both reduced postmeal exposure to insulin (32) and decreased insulin sensitivity (33) may have contributed to lowered postprandial LPL activity in subjects consuming fructose compared with those consuming glucose.”
• Sugar consumption, metabolic disease and obesity: The state of the controversy (2015, neutral): “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 wi”
• The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome (2010, background): “Direct effects of fructose on the central nervous system (CNS) include stimulation of hormones that stimulate appetite and reward”
• Mechanisms (2019, neutral): “Concurring with the results of 2 other studies (33, 34), the results of the present study showed that fructose potentiates postprandial lipemia in the acute setting.”
• Sugar, Uric Acid, and the Etiology of Diabetes and Obesity (2013, background): “The intake of fructose is not effective in stimulating insulin and leptin secretion in humans, and hence may not induce a satiety response (6).”
• Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. (2007, background): “First, Havel’s group (54) conducted a clinical study that found that fructose may not cause the level of satiety equivalent to that of a glucose-based meal.”