Effects of Adult Usage of Low-Calorie Sweeteners

Kidane Aaron^*
*Correspondence: Kidane Aaron, Department of Pharmacy, University of Asmara, Asmara, Eritrea, Email:

Description

Early Western diet consumption is associated with higher caloric intake, an increased risk of obesity, and adult metabolic dysfunction. The underlying nutritive mechanisms that mediate these effects are poorly understood due to the fact that established rodent obesogenic diet models differ from healthy control diets in two main ways. 1) Increased intake of sugar and dietary fat, especially saturated fatty acids. It is essential to comprehend the long-term effects of habitual sugar consumption in early life without concurrent elevated dietary fat on eating patterns and body weight regulation in adulthood because children consume the most sugar of any age group and SSBs are a major source of sugar in their diets [1].

In light of the alarming rise in childhood obesity and nutrition-related comorbidities, dietary and lifestyle interventions to better support healthy growth trajectories have received more attention. One of these methods is to reduce sugar intake. At least theoretically, consuming foods and beverages in which low-calorie sweeteners (LCSs) have completely or partially replaced sugars can reduce sugar consumption while maintaining a pleasant sweetness; However, inconsistent evidence from human and rodent models challenges the efficacy of LCSs for weight management and energy balance maintenance. It is unclear how adult energy balance control is affected by sugar or LCS consumption in the early stages of development. The voluntary consumption of sucrose solution in early life, which modeled a concentration and daily caloric levels commonly consumed by humans, had no effect on energy intake, body weight, or glucose homeostasis when compared to a cafeteria-style Western diet (CAF) during adulthood. When LCSs consumed a CAF diet as adults, early habitual consumption of ACE-K, but not stevia, disrupted the energy balance, with significant gender-dependent effects. More specifically, male and female Expert K-uncovered rodents consumed fewer calories than controls during the adult CAF period, but the females exhibited a significant weight loss, whereas the males did not. This sexdependent disparity in ACE-K rats was most likely caused by males' decreased mRNA expression of BMP8B and UCP1 in brown adipose tissue (BAT), whereas females' expression of these thermogenic activity markers was unaffected.

It was surprising that early sugar consumption had no effect on energy balance parameters, given the "developmental programming hypothesis," which asserts that early life is a crucial period for programming energy balance and metabolic health later in life. Adolescent consumption of either ad libitum or 5% kcals from sugar of comparable sugar solutions (HFCS or sucrose) in rats did not alter caloric intake or body weight in early adulthood, despite causing long-lasting memory impairments and changes to the micro biome. The current findings, when taken together with the previous ones, suggest that early sugar consumption may have a greater long-term impact on memory function than on ingestive and metabolic outcomes. Male mice had higher body weights than controls after four weeks of adult ACE-K consumption, whereas female mice did not differ from controls. These variations were caused by changes in the community of gut bacteria and functional genes related to energy metabolism. Our most recent work with the early life LCS model revealed no significant differences in the gut microbiome. However, adult consumption of the CAF diet was not included in the previous study. Despite the fact that our current study and previous work both support the hypothesis that consumption of ACE-K is linked to energy balance dysregulation, which is more pronounced in males [2-4].

The impact of early stevia consumption, with a significant increase in admission of the sweet refreshment observed for females during adult CAF diet openness in comparison to controls, is an especially notable finding from the current study. However, males exposed to stevia did not differ in any other way, and females exposed to stevia consumed the same number of calories as controls. Past disclosures show that high parcels of stevia achieve body weight diminishes beginning a month and a half after transparency in adult female rodents, which suggests that a more broadened season of receptiveness and a higher part than the ADI. In diabetic rats, high doses of stevia were found to have similar weight loss effects and notable anti-diabetic properties. In vitro studies suggest that stevia may also disrupt the endocrine system, but human or rodent models have not yet been used to test this hypothesis. Regardless, our data indicate that stevia consumption in childhood had no effect on overall energy balance when consumed within the federally recommended daily limits, but that it increased sex-dependently the consumption of sugary beverages in adulthood. However, the adult CAF diet exposure in this study included healthy food and food alternatives other than a sugar solution, which may have affected the total amount of sugar consumed. Importantly, our experiments used voluntary consumption of LCSs that was restricted in accordance with the recommended federal daily limits, in contrast to the majority of previous rodent LCS research that used excessive and involuntary consumption. As a result, the findings are more applicable to humans. These findings highlight the significance of gender differences in terms of the effects of LCS consumption on energy balance and identify early exposure asa a crucial period for lasting metabolic effects [5].

According to our findings, consuming low-calorie sweeteners on a regular basis during the early stages of development influences adult energy balance outcomes. For example, consuming ACE-K was associated with decreased expression of genes related to thermogenesis in adult males, while consuming stevia was associated with increased consumption of sugary beverages in adult females.

Acknowledgement

None.

Conflict of Interest

The authors declare that there is no conflict of interest associated with this manuscript.

References

1. Noble, Emily E., Ted M. Hsu, Joanna Liang and Scott E. Kanoski. "Early-life sugar consumption has long-term negative effects on memory function in male rats." Nutr Neurosci 22 (2019): 273-283.

Google Scholar, Crossref, Indexed at

2. Noble, Emily E., Christine A. Olson, Elizabeth Davis and Linda Tsan. "Gut microbial taxa elevated by dietary sugar disrupt memory function." Transl Psychiatry 11 (2021): 1-16.

Google Scholar, Crossref, Indexed at

3. Tsan, Linda, Shan Sun, Anna MR Hayes and Lana Bridi. "Early life Western diet-induced memory impairments and gut microbiome changes in female rats are long-lasting despite healthy dietary intervention." Nutr Neurosci 25 (2022): 2490-2506.

Google Scholar, Crossref, Indexed at

4. Belzung, Catherine and Guy Griebel. "Measuring normal and pathological anxiety-like behaviour in mice: A review." Behav Brain Res 125 (2001): 141-149.

Google Scholar, Crossref

5. Fedorenko, Andriy, Polina V. Lishko and Yuriy Kirichok. "Mechanism of fatty-acid-dependent UCP1 uncoupling in brown fat mitochondria." Cell 151 (2012): 400-413.

Google Scholar, Crossref