A new study was recently published in Calcified Tissue International which compared the effects of high-fat and high-fructose diets on various outcomes including visceral and subcutaneous fat deposition, de novo lipogenesis, plasma glucose, plasma leptin, plasma insulin, and bone architecture and stiffness.

The experiment conducted by Jatkar et al. utilized 30 male mice divided into three group of ten. The control group (SC) received a standard chow diet. The high-fructose group (CH) received a standard chow diet with 10% weight per volume powered fructose diluted into their drinking water. The high-fat group (HF) received a diet which provided 45% of calories from fat. The mice were provided their respective diets for 15 weeks. Two weeks prior to their sacrifice, mice were also given an isotope tracer of deuterium in their water to assess lipid synthesis.

Researchers found that mice on the HF diet consumed less food and fewer calories overall than both the CH and SC mice. The difference in intake was not statistically significant between CH and SC mice. Interestingly, by the end of the 15 week treatment, the body mass index (BMI) of mice in the HF diet group was approximately 10% greater compared to the SC but was not significantly greater than the BMI of CH mice. Similarly, the epididymal fat pads of mice fed the HF diet were significantly greater than those in the SC group. Conversely, epididymal fat pads for the CH mice were 57% smaller compared to those on the SC diet. Furthermore, thermogenic brown fat pads were 156% larger for the CH mice compared to the SC group and 65% greater compared to the HF mice.

Fasting glucose and plasma insulin levels were not significantly different between groups. Plasma leptin levels of the HF fed mice were approximately four-fold greater than the SC fed mice and two-fold greater than the CH fed mice. Fatty acid synthesis was assessed in the liver, kidney, white adipose tissue, and brown adipose tissue. Lipid synthesis in all tissues was significantly lower in the HF group compared to the SC group. Similarly, fatty acid synthesis in all tissues was significantly lower in the HF group compared to the CH group.

Next, researchers examined the effects of the diet interventions on bone morphology. It was discovered that when compared to SC and CH diets, a HF diet resulted in significantly reduced cortical bone volume fraction, cortical thickness, and tissue mineral density but did not alter total cortical area. The HF diet treatment also resulted in altered trabecular bone morphology; the HF group had reduced trabecular bone volume fraction and greater structural model index compared to both the SC and CH groups. Lastly, researchers noted that bone elastic modulus was 22% smaller in the CH fed mice compared to the HF fed mice.

Researchers concluded, “In the absence of the protective effect of increased load bearing, chronic high-fat consumption was detrimental to bone mass and its architecture as well as tissue density. The high-fat diet also increase deposition of subcutaneous and visceral fat stores and reduced fractional new synthesis of lipids. In contrast, chronic consumption of fructose at moderate levels did not impact bone and fat mass, new lipid synthesis or other indicators of metabolic health but elevated interscapular brown adipose tissue mass. It also compromised bone’s internal stiffness when compared to the high-fat group.”

The post Diets High in Fat or Fructose Differentially Modulate Bone Health and Lipid Metabolism appeared first on FructoseFacts.

A review was recently published in Nutrients which examined the relationship between early life exposure to fructose and cardiometabolic outcomes in offspring. Reviewers cited a number studies which associated fructose intake with various health outcomes such as insulin resistance, elevated low density lipoprotein cholesterol, elevated triglycerides, obesity, type 2 diabetes, cardiovascular disease, non-fatal myocardial infarction, and fatal coronary heart disease.

Reviewers then noted that there is limited human data on the effects of excessive fructose consumption during the early stages of life to include gestation, lactation, and infancy. Zheng et al. cited two cohort studies; the first found that intake of fructose from natural sources reduced the risk of pre-eclampsia whereas the second study found that sugar sweetened beverage intake was associated with increased risk of pre-term delivery.

Reviewers also examined the relevant literature on fructose consumption in rodent models. While results varied between experiments, reviewers noted several points. First, the offspring of dams consuming high fructose diets experienced elevated circulating plasma fructose, elevated plasma leptin, elevated plasma insulin, obesity, hypertension, insulin resistance, increased rates of fatty liver, increased free fatty acids, greater visceral adipose tissue stores, changes in stress-response axis, changes in nocturnal blood pressure, and hypertriglyceridemia. Additionally, the dams consuming high fructose diets experienced increased food intake, decreased water intake, sex-specific effects on placental growth and fetal and neonatal metabolic profiles, alterations in the secondary sex ratio and reduced fertility.

Lastly, reviewers outlined proposed mechanisms for the observed effects in both mothers and offspring. Reviewers first described the ability of fructose to be rapidly metabolized in the liver which can promote de novo lipogenesis which in turn, promotes dyslipidemia. The second suggested mechanism comes from a rodent study in which maternal consumption of fructose during lactation resulted in “decreased hypothalamic sensitivity to exogenous leptin, enhanced food intake, and decreased several anorexigenic signals…in the off spring.” The last proposed mechanism suggests that offspring consuming high-fructose diets demonstrate enhanced expression of glucose transporter 5. Reviewers noted “it is still unclear whether the impacts on the offspring are direct effects of fructose transfer through the placenta or the mother’s milk, or due to adaptive responses and altered maternal metabolism.”

Reviewers concluded, “One important point that should be taken into consideration is that early life fructose exposure may determine the susceptibility of long-term metabolic diseases in offspring. However, limited data suggest that the offspring would be protected from these well-known adverse effects during early life.”

The post Early Life Fructose Exposure and Its Implications for Long-Term Cardiometabolic Health in Offspring appeared first on FructoseFacts.