Sucrose and polysaccharide induced obesity in the rat

Sclafani, Anthony; Xenakis, Steven

doi:10.1016/0031-9384(84)90125-2

Cited by 70 publications

(27 citation statements)

References 24 publications

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“…27 Moreover, beverage intakes seem to be less precisely regulated than solid foods in humans [28][29][30][31] and animals. [32][33][34][35][36] In young children, energy imbalances as subtle as 125.82 kJ/day can promote overweight, 37 which could be easily achieved by juice intake given that a standard 6-to 8-oz. fruit juice box has ϳ418.4 kJ.…”

Section: Discussionmentioning

confidence: 99%

Fruit Juice Intake Predicts Increased Adiposity Gain in Children From Low-Income Families: Weight Status-by-Environment Interaction

et al. 2006

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Section: Discussionmentioning

confidence: 99%

Fruit Juice Intake Predicts Increased Adiposity Gain in Children From Low-Income Families: Weight Status-by-Environment Interaction

et al. 2006

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“…For example, these studies showed that high glucose consumption causes an increase in body weight and abdominal fat associated with an increased protein oxidation induced by hyperglycemia, and that carbohydrate-induced obesity is not dependent on the sweet taste of carbohydrates. 6,21,22 Another important mechanism through which the intake of carbohydrates and particularly a glucose intake may be regulated is through a modulation of the intestinal serotonergic system. Indeed, previous studies have indicated that intestinal 5-HT3R might be involved in the detection and control of carbohydrate intake, such as glucose.…”

Section: Discussionmentioning

confidence: 99%

Treatment with the 5-HT3 antagonist tropisetron modulates glucose-induced obesity in mice

et al. 2009

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Objective: Sugar consumption has increased markedly over the last few decades and parallels the dramatic increase in overweight and obesity. Data obtained from animal studies suggest that the intestinal serotonergic system and herein particularly the serotonin receptor 3 (5-HT3R) may be involved in sugar detection and short-term control of food intake. Using a mouse model, we tested the hypothesis that blocking 5-HT3R prevents the development of sugar-induced obesity. Design: For 8 weeks, C57BL/J6 mice were offered either water containing 30% glucose or plain water in addition to normal chow. The effect of oral treatment with the 5-HT3R antagonist, tropisetron (0.2 mg kg À1 body weight), on body weight and caloric intake was studied. Results: Total caloric intake and weight gain were significantly increased in mice fed glucose compared with the control group. Tropisetron treatment reduced intestinal motility and almost completely blocked weight gain associated with glucose feeding; however, total caloric intake was not affected. The effect of tropisetron was not associated with a decreased expression of the intestinal and hepatic glucose transporters, SGLT1 (sodium-dependent glucose cotransporter) and Glut2 (glucose transporter 2); instead, the expression of these transporters was slightly increased by the 5-HT3R antagonist. However, expressions of carbohydrate responsive element binding protein and fatty acid synthase, as well as triglyceride levels in the liver were only enhanced in mice fed glucose, but remained unchanged at the level of the control group when mice were treated concomitantly with tropisetron. At the same time, b-hydroxybutyrate dehydrogenase mRNA expression and plasma levels of ketone bodies were significantly increased. Conclusion: Our results suggest that 5-HT3R is a new target for the modulation of hepatic glucose metabolism and for the prevention of obesity.

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“…However, there was no difference in body weight, although percentage body fat was increased. A very similar outcome – elevated caloric intake but no effect on growth – was recorded in another study of weanling rats allowed access to 32% sucrose [45]. However, the variability in outcome between different studies is well illustrated by the outcome of feeding adult rats (up to 210 days of age) with the same concentration of sucrose solution, where no increase in total caloric intake was evident [46].…”

Section: Diet and Leptin Resistancementioning

confidence: 63%

Dietary Factors Affect Food Reward and Motivation to Eat

Pandit¹,

Mercer²,

Overduin³

et al. 2012

Obes Facts

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The propensity to indulge in unhealthy eating and overconsumption of palatable food is a crucial determinant in the rising prevalence of obesity in today’s society. The tendency to consume palatable foods in quantities that exceed energy requirements has been linked to an addiction-like process. Although the existence of ‘food addiction’ has not been conclusively proven, evidence points to alterations in the brain reward circuitry induced by overconsumption of palatable foods that are similar to those seen in drug addiction. The diet-induced obesity paradigm is a common procedure to replicate features of human obesity in rodents. Here we review data on the effect of various obesogenic diets (high-fat, Ensure™, cafeteria type, sucrose) on the extent of leptin resistance, hypothalamic-neuropeptidergic adaptations and changes in feeding behavior. We also discuss to what extent such diets and properties such as macronutrient composition, physical structure, sensory stimuli, and post-ingestive effects influence the brain-reward pathways. Understanding the interaction between individual components of diets, feeding patterns, and brain reward pathways could facilitate the design of diets that limit overconsumption and prevent weight gain.

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Sucrose and polysaccharide induced obesity in the rat

Cited by 70 publications

References 24 publications

Fruit Juice Intake Predicts Increased Adiposity Gain in Children From Low-Income Families: Weight Status-by-Environment Interaction

Fruit Juice Intake Predicts Increased Adiposity Gain in Children From Low-Income Families: Weight Status-by-Environment Interaction

Treatment with the 5-HT3 antagonist tropisetron modulates glucose-induced obesity in mice

Dietary Factors Affect Food Reward and Motivation to Eat

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