The Experts below are selected from a list of 273 Experts worldwide ranked by ideXlab platform

Veronika Somoza - One of the best experts on this subject based on the ideXlab platform.

  • noncaloric sweeteners induce peripheral serotonin secretion via the t1r3 dependent pathway in human gastric parietal tumor cells hgt 1
    Journal of Agricultural and Food Chemistry, 2018
    Co-Authors: Muhammet Zopun, Barbara Lieder, Annkatrin Holik, Joachim Hans, Veronika Somoza
    Abstract:

    The role of sweet taste in energy intake and satiety regulation is still controversial. Noncaloric artificial sweeteners (NCSs) are thought to help reduce energy intake, although little is known about their impact on the satiating neurotransmitter serotonin (5-HT). In the gastrointestinal (GI) tract, 5-HT regulates gastric acid secretion and gastric motility, both part of the complex network of mechanisms regulating food intake and satiety. This study demonstrated a stimulating impact compared to controls (100%) on 5-HT release in human gastric tumor cells (HGT-1) by the NCSs cyclamate (50 mM, 157% ± 6.3%), Acesulfame Potassium (Ace K, 50 mM, 197% ± 8.6%), saccharin (50 mM, 147% ± 6.7%), sucralose (50 mM, 194% ± 11%), and neohesperidin dihydrochalcone (NHDC, 1 mM, 201% ± 13%). Although these effects were not associated with the sweet taste intensity of the NCSs tested, involvement of the sweet receptor subunit T1R3 in the NCS-evoked response was demonstrated by mRNA expression of TAS1R3, co-incubation exp...

  • Noncaloric Sweeteners Induce Peripheral Serotonin Secretion via the T1R3-Dependent Pathway in Human Gastric Parietal Tumor Cells (HGT-1)
    2018
    Co-Authors: Muhammet Zopun, Barbara Lieder, Annkatrin Holik, Joachim Hans, Jakop P. Ley, Veronika Somoza
    Abstract:

    The role of sweet taste in energy intake and satiety regulation is still controversial. Noncaloric artificial sweeteners (NCSs) are thought to help reduce energy intake, although little is known about their impact on the satiating neurotransmitter serotonin (5-HT). In the gastrointestinal (GI) tract, 5-HT regulates gastric acid secretion and gastric motility, both part of the complex network of mechanisms regulating food intake and satiety. This study demonstrated a stimulating impact compared to controls (100%) on 5-HT release in human gastric tumor cells (HGT-1) by the NCSs cyclamate (50 mM, 157% ± 6.3%), Acesulfame Potassium (Ace K, 50 mM, 197% ± 8.6%), saccharin (50 mM, 147% ± 6.7%), sucralose (50 mM, 194% ± 11%), and neohesperidin dihydrochalcone (NHDC, 1 mM, 201% ± 13%). Although these effects were not associated with the sweet taste intensity of the NCSs tested, involvement of the sweet receptor subunit T1R3 in the NCS-evoked response was demonstrated by mRNA expression of TAS1R3, co-incubation experiments using the T1R3 receptor antagonist lactisole, and a TAS1R3 siRNA knockdown approach. Analysis of the downstream signaling revealed activation of the cAMP/ERK/Ca2+ cascade. Co-treatment experiments with 10 mM glucose enhanced the 5-HT release induced by cyclamate, Ace K, saccharin, and sucralose, thereby supporting the enhancing effect of glucose on a NCS-mediated response. Overall, the results obtained identify NCSs as potent inducers of 5-HT release via T1R3 in human gastric parietal cells in culture and warrant in vivo studies to demonstrate their efficacy

Kristina I Rother - One of the best experts on this subject based on the ideXlab platform.

  • consumption of diet soda sweetened with sucralose and Acesulfame Potassium alters inflammatory transcriptome pathways in females with overweight and obesity
    Molecular Nutrition & Food Research, 2020
    Co-Authors: Allison C Sylvetsky, Peter Walter, Sabyasachi Sen, Patrick Merkel, Fiona J Dore, David L Stern, Curtis J Henry, Hongyi Cai, Keith A Crandall, Kristina I Rother
    Abstract:

    Scope Low-calorie sweetener (LCS) consumption is associated with metabolic disease in observational studies. However, physiologic mechanisms underlying LCS-induced metabolic impairments in humans are unclear. This study is aimed at identifying molecular pathways in adipose impacted by LCSs. Methods and results Seven females with overweight or obesity, who did not report LCS use, consumed 12 ounces of diet soda containing sucralose and Acesulfame-Potassium (Ace-K) three times daily for 8 weeks. A subcutaneous adipose biopsy from the left abdomen and a fasting blood sample were collected at baseline and post-intervention. Global gene expression were assessed using RNA-sequencing followed by functional pathway analysis. No differences in circulating metabolic or inflammatory biomarkers were observed. However, ANOVA detected 828 differentially expressed annotated genes after diet soda consumption (p Conclusion Consumption of diet soda with sucralose and Ace-K alters inflammatory transcriptomic pathways (e.g., NF-κB signaling) in subcutaneous adipose tissue but does not significantly alter circulating biomarkers. Findings highlight the need to examine molecular and metabolic effects of LCS exposure in a larger randomized control trial for a longer duration.

  • consumption of diet soda sweetened with sucralose and Acesulfame Potassium alters inflammatory transcriptome pathways in females with overweight and obesity
    Molecular Nutrition & Food Research, 2020
    Co-Authors: Allison C Sylvetsky, Kristina I Rother, Peter Walter, Patrick Merkel, Curtis J Henry, Keith A Crandall, F Dore, D B Stern, M J Hubal
    Abstract:

    SCOPE: Low-calorie sweetener (LCS) consumption is associated with metabolic disease in observational studies. However, physiologic mechanisms underlying LCS-induced metabolic impairments in humans are unclear. This study aimed to identify molecular pathways in adipose impacted by LCS consumption. METHODS AND RESULTS: Seven females with overweight or obesity, who did not report LCS use, consumed 12-ounces of diet soda containing sucralose and Acesulfame-Potassium (Ace-K) three times daily for 8-weeks. A subcutaneous adipose biopsy from the left abdomen and fasting blood sample were collected at baseline and post-intervention. Global gene expression changes were assessed using RNA-sequencing followed by functional pathway analysis. No differences in circulating metabolic or inflammatory biomarkers were observed. However, ANOVA detected 828 differentially expressed annotated genes after diet soda consumption (p<0.05), including transcripts for inflammatory cytokines including interleukins and tumor-necrosis-family members. Fifty-eight of 140 canonical pathways represented in pathway analyses regulate inflammation, and several key upstream regulators of inflammation (e.g. TNF-alpha) were also represented. CONCLUSION: Consumption of diet soda with sucralose and Ace-K altered inflammatory transcriptomic pathways (e.g. NF-kappaB signaling) in subcutaneous adipose tissue but did not significantly alter circulating biomarkers. These findings highlight the need to examine molecular and metabolic effects of LCS exposure in a larger randomized control trial for a longer duration. This article is protected by copyright. All rights reserved.

  • Pharmacokinetics of Sucralose and Acesulfame-Potassium in Breast Milk Following Ingestion of Diet Soda.
    Journal of Pediatric Gastroenterology and Nutrition, 2018
    Co-Authors: Kristina I Rother, Allison C Sylvetsky, Peter Walter, H. Martin Garraffo, David A. Fields
    Abstract:

    Objective: The aim of this study was to determine sucralose and Acesulfame-Potassium (ace-K) pharmacokinetics in breast milk following maternal ingestion of a diet soda. Methods: Thirty-four exclusively breast-feeding women (14 normal-weight, 20 obese) consumed 12 ounces of Diet Rite Cola, sweetened with 68-mg sucralose and 41-mg ace-K, before a standardized breakfast meal. Habitual non-nutritional sweeteners intake was assessed via a diet questionnaire. Breast milk was collected from the same breast before beverage ingestion and hourly for 6 hours. Results: Owing to one mother having extremely high concentrations, peak sucralose and Acesulfame-Potassium concentrations following ingestion of diet soda ranged from 4.0 to 7387.9 ng/mL (median peak 8.1 ng/mL) and 299.0 to 4764.2 ng/mL (median peak 945.3 ng/mL), respectively. Conclusions: Ace-K and sucralose transfer into breast milk following ingestion of a diet soda. Future research should measure concentrations after repeated exposure and determine whether chronic ingestion of sucralose and Acesulfame-Potassium via the breast milk has clinically relevant health consequences.

  • plasma concentrations of sucralose in children and adults
    Toxicological & Environmental Chemistry, 2017
    Co-Authors: Allison C Sylvetsky, Viviana Bauman, Jenny E Blau, Martin H Garraffo, Peter Walter, Kristina I Rother
    Abstract:

    ABSTRACTWe aimed to measure concentrations of the commonly used artificial sweetener sucralose, following ingestion of doses reflecting a range of consumption and to compare concentrations in children and adults. Eleven adults consumed 355 mL water containing 0 mg (control), 68, 170, or 250 mg sucralose (equivalent to 1–4 diet sodas). A second group of adults (n = 11) consumed 355 mL Diet Rite Cola™ (68 mg sucralose and 41 mg Acesulfame-Potassium (ace-K)) or 68 mg sucralose and 41 mg ace-K in seltzer. Beverages were provided at separate visits in randomized order, prior to an oral glucose tolerance test. Eleven children consumed 0 or 68 mg sucralose in 240 mL water, in an identical study design. Blood was collected before beverage ingestion and serially for 120 min. Sucralose doses (corrected for weight) resulted in similar plasma concentrations in children and adults. Concentrations were comparable whether sucralose was administered in water, combined with ace-K, or in diet soda. Due to their lower body ...

  • plasma concentrations of sucralose in children and adults
    Toxicological & Environmental Chemistry, 2017
    Co-Authors: Allison C Sylvetsky, Viviana Bauman, Jenny E Blau, Martin H Garraffo, Peter Walter, Kristina I Rother
    Abstract:

    ABSTRACTWe aimed to measure concentrations of the commonly used artificial sweetener sucralose, following ingestion of doses reflecting a range of consumption and to compare concentrations in children and adults. Eleven adults consumed 355 mL water containing 0 mg (control), 68, 170, or 250 mg sucralose (equivalent to 1–4 diet sodas). A second group of adults (n = 11) consumed 355 mL Diet Rite Cola™ (68 mg sucralose and 41 mg Acesulfame-Potassium (ace-K)) or 68 mg sucralose and 41 mg ace-K in seltzer. Beverages were provided at separate visits in randomized order, prior to an oral glucose tolerance test. Eleven children consumed 0 or 68 mg sucralose in 240 mL water, in an identical study design. Blood was collected before beverage ingestion and serially for 120 min. Sucralose doses (corrected for weight) resulted in similar plasma concentrations in children and adults. Concentrations were comparable whether sucralose was administered in water, combined with ace-K, or in diet soda. Due to their lower body ...

Muhammet Zopun - One of the best experts on this subject based on the ideXlab platform.

  • noncaloric sweeteners induce peripheral serotonin secretion via the t1r3 dependent pathway in human gastric parietal tumor cells hgt 1
    Journal of Agricultural and Food Chemistry, 2018
    Co-Authors: Muhammet Zopun, Barbara Lieder, Annkatrin Holik, Joachim Hans, Veronika Somoza
    Abstract:

    The role of sweet taste in energy intake and satiety regulation is still controversial. Noncaloric artificial sweeteners (NCSs) are thought to help reduce energy intake, although little is known about their impact on the satiating neurotransmitter serotonin (5-HT). In the gastrointestinal (GI) tract, 5-HT regulates gastric acid secretion and gastric motility, both part of the complex network of mechanisms regulating food intake and satiety. This study demonstrated a stimulating impact compared to controls (100%) on 5-HT release in human gastric tumor cells (HGT-1) by the NCSs cyclamate (50 mM, 157% ± 6.3%), Acesulfame Potassium (Ace K, 50 mM, 197% ± 8.6%), saccharin (50 mM, 147% ± 6.7%), sucralose (50 mM, 194% ± 11%), and neohesperidin dihydrochalcone (NHDC, 1 mM, 201% ± 13%). Although these effects were not associated with the sweet taste intensity of the NCSs tested, involvement of the sweet receptor subunit T1R3 in the NCS-evoked response was demonstrated by mRNA expression of TAS1R3, co-incubation exp...

  • Noncaloric Sweeteners Induce Peripheral Serotonin Secretion via the T1R3-Dependent Pathway in Human Gastric Parietal Tumor Cells (HGT-1)
    2018
    Co-Authors: Muhammet Zopun, Barbara Lieder, Annkatrin Holik, Joachim Hans, Jakop P. Ley, Veronika Somoza
    Abstract:

    The role of sweet taste in energy intake and satiety regulation is still controversial. Noncaloric artificial sweeteners (NCSs) are thought to help reduce energy intake, although little is known about their impact on the satiating neurotransmitter serotonin (5-HT). In the gastrointestinal (GI) tract, 5-HT regulates gastric acid secretion and gastric motility, both part of the complex network of mechanisms regulating food intake and satiety. This study demonstrated a stimulating impact compared to controls (100%) on 5-HT release in human gastric tumor cells (HGT-1) by the NCSs cyclamate (50 mM, 157% ± 6.3%), Acesulfame Potassium (Ace K, 50 mM, 197% ± 8.6%), saccharin (50 mM, 147% ± 6.7%), sucralose (50 mM, 194% ± 11%), and neohesperidin dihydrochalcone (NHDC, 1 mM, 201% ± 13%). Although these effects were not associated with the sweet taste intensity of the NCSs tested, involvement of the sweet receptor subunit T1R3 in the NCS-evoked response was demonstrated by mRNA expression of TAS1R3, co-incubation experiments using the T1R3 receptor antagonist lactisole, and a TAS1R3 siRNA knockdown approach. Analysis of the downstream signaling revealed activation of the cAMP/ERK/Ca2+ cascade. Co-treatment experiments with 10 mM glucose enhanced the 5-HT release induced by cyclamate, Ace K, saccharin, and sucralose, thereby supporting the enhancing effect of glucose on a NCS-mediated response. Overall, the results obtained identify NCSs as potent inducers of 5-HT release via T1R3 in human gastric parietal cells in culture and warrant in vivo studies to demonstrate their efficacy

George L Kellett - One of the best experts on this subject based on the ideXlab platform.

  • sweet taste receptors in rat small intestine stimulate glucose absorption through apical glut2
    The Journal of Physiology, 2007
    Co-Authors: Oliver J Mace, Julie Affleck, Nick Patel, George L Kellett
    Abstract:

    Natural sugars and artificial sweeteners are sensed by receptors in taste buds. T2R bitter and T1R sweet taste receptors are coupled through G-proteins, alpha-gustducin and transducin, to activate phospholipase C beta2 and increase intracellular calcium concentration. Intestinal brush cells or solitary chemosensory cells (SCCs) have a structure similar to lingual taste cells and strongly express alpha-gustducin. It has therefore been suggested over the last decade that brush cells may participate in sugar sensing by a mechanism analogous to that in taste buds. We provide here functional evidence for an intestinal sensing system based on lingual taste receptors. Western blotting and immunocytochemistry revealed that all T1R members are expressed in rat jejunum at strategic locations including Paneth cells, SCCs or the apical membrane of enterocytes; T1Rs are colocalized with each other and with alpha-gustducin, transducin or phospholipase C beta2 to different extents. Intestinal glucose absorption consists of two components: one is classical active Na+-glucose cotransport, the other is the diffusive apical GLUT2 pathway. Artificial sweeteners increase glucose absorption in the order Acesulfame Potassium approximately sucralose > saccharin, in parallel with their ability to increase intracellular calcium concentration. Stimulation occurs within minutes by an increase in apical GLUT2, which correlates with reciprocal regulation of T1R2, T1R3 and alpha-gustducin versus T1R1, transducin and phospholipase C beta2. Our observation that artificial sweeteners are nutritionally active, because they can signal to a functional taste reception system to increase sugar absorption during a meal, has wide implications for nutrient sensing and nutrition in the treatment of obesity and diabetes.

  • sweet taste receptors in rat small intestine stimulate glucose absorption through apical glut2
    The Journal of Physiology, 2007
    Co-Authors: Oliver J Mace, Julie Affleck, Nick Patel, George L Kellett
    Abstract:

    Natural sugars and artificial sweeteners are sensed by receptors in taste buds. T2R bitter and T1R sweet taste receptors are coupled through G-proteins, α-gustducin and transducin, to activate phospholipase C β2 and increase intracellular calcium concentration. Intestinal brush cells or solitary chemosensory cells (SCCs) have a structure similar to lingual taste cells and strongly express α-gustducin. It has therefore been suggested over the last decade that brush cells may participate in sugar sensing by a mechanism analogous to that in taste buds. We provide here functional evidence for an intestinal sensing system based on lingual taste receptors. Western blotting and immunocytochemistry revealed that all T1R members are expressed in rat jejunum at strategic locations including Paneth cells, SCCs or the apical membrane of enterocytes; T1Rs are colocalized with each other and with α-gustducin, transducin or phospholipase C β2 to different extents. Intestinal glucose absorption consists of two components: one is classical active Na+–glucose cotransport, the other is the diffusive apical GLUT2 pathway. Artificial sweeteners increase glucose absorption in the order Acesulfame Potassium ∼ sucralose > saccharin, in parallel with their ability to increase intracellular calcium concentration. Stimulation occurs within minutes by an increase in apical GLUT2, which correlates with reciprocal regulation of T1R2, T1R3 and α-gustducin versus T1R1, transducin and phospholipase C β2. Our observation that artificial sweeteners are nutritionally active, because they can signal to a functional taste reception system to increase sugar absorption during a meal, has wide implications for nutrient sensing and nutrition in the treatment of obesity and diabetes.

Allison C Sylvetsky - One of the best experts on this subject based on the ideXlab platform.

  • consumption of diet soda sweetened with sucralose and Acesulfame Potassium alters inflammatory transcriptome pathways in females with overweight and obesity
    Molecular Nutrition & Food Research, 2020
    Co-Authors: Allison C Sylvetsky, Peter Walter, Sabyasachi Sen, Patrick Merkel, Fiona J Dore, David L Stern, Curtis J Henry, Hongyi Cai, Keith A Crandall, Kristina I Rother
    Abstract:

    Scope Low-calorie sweetener (LCS) consumption is associated with metabolic disease in observational studies. However, physiologic mechanisms underlying LCS-induced metabolic impairments in humans are unclear. This study is aimed at identifying molecular pathways in adipose impacted by LCSs. Methods and results Seven females with overweight or obesity, who did not report LCS use, consumed 12 ounces of diet soda containing sucralose and Acesulfame-Potassium (Ace-K) three times daily for 8 weeks. A subcutaneous adipose biopsy from the left abdomen and a fasting blood sample were collected at baseline and post-intervention. Global gene expression were assessed using RNA-sequencing followed by functional pathway analysis. No differences in circulating metabolic or inflammatory biomarkers were observed. However, ANOVA detected 828 differentially expressed annotated genes after diet soda consumption (p Conclusion Consumption of diet soda with sucralose and Ace-K alters inflammatory transcriptomic pathways (e.g., NF-κB signaling) in subcutaneous adipose tissue but does not significantly alter circulating biomarkers. Findings highlight the need to examine molecular and metabolic effects of LCS exposure in a larger randomized control trial for a longer duration.

  • consumption of diet soda sweetened with sucralose and Acesulfame Potassium alters inflammatory transcriptome pathways in females with overweight and obesity
    Molecular Nutrition & Food Research, 2020
    Co-Authors: Allison C Sylvetsky, Kristina I Rother, Peter Walter, Patrick Merkel, Curtis J Henry, Keith A Crandall, F Dore, D B Stern, M J Hubal
    Abstract:

    SCOPE: Low-calorie sweetener (LCS) consumption is associated with metabolic disease in observational studies. However, physiologic mechanisms underlying LCS-induced metabolic impairments in humans are unclear. This study aimed to identify molecular pathways in adipose impacted by LCS consumption. METHODS AND RESULTS: Seven females with overweight or obesity, who did not report LCS use, consumed 12-ounces of diet soda containing sucralose and Acesulfame-Potassium (Ace-K) three times daily for 8-weeks. A subcutaneous adipose biopsy from the left abdomen and fasting blood sample were collected at baseline and post-intervention. Global gene expression changes were assessed using RNA-sequencing followed by functional pathway analysis. No differences in circulating metabolic or inflammatory biomarkers were observed. However, ANOVA detected 828 differentially expressed annotated genes after diet soda consumption (p<0.05), including transcripts for inflammatory cytokines including interleukins and tumor-necrosis-family members. Fifty-eight of 140 canonical pathways represented in pathway analyses regulate inflammation, and several key upstream regulators of inflammation (e.g. TNF-alpha) were also represented. CONCLUSION: Consumption of diet soda with sucralose and Ace-K altered inflammatory transcriptomic pathways (e.g. NF-kappaB signaling) in subcutaneous adipose tissue but did not significantly alter circulating biomarkers. These findings highlight the need to examine molecular and metabolic effects of LCS exposure in a larger randomized control trial for a longer duration. This article is protected by copyright. All rights reserved.

  • Pharmacokinetics of Sucralose and Acesulfame-Potassium in Breast Milk Following Ingestion of Diet Soda.
    Journal of Pediatric Gastroenterology and Nutrition, 2018
    Co-Authors: Kristina I Rother, Allison C Sylvetsky, Peter Walter, H. Martin Garraffo, David A. Fields
    Abstract:

    Objective: The aim of this study was to determine sucralose and Acesulfame-Potassium (ace-K) pharmacokinetics in breast milk following maternal ingestion of a diet soda. Methods: Thirty-four exclusively breast-feeding women (14 normal-weight, 20 obese) consumed 12 ounces of Diet Rite Cola, sweetened with 68-mg sucralose and 41-mg ace-K, before a standardized breakfast meal. Habitual non-nutritional sweeteners intake was assessed via a diet questionnaire. Breast milk was collected from the same breast before beverage ingestion and hourly for 6 hours. Results: Owing to one mother having extremely high concentrations, peak sucralose and Acesulfame-Potassium concentrations following ingestion of diet soda ranged from 4.0 to 7387.9 ng/mL (median peak 8.1 ng/mL) and 299.0 to 4764.2 ng/mL (median peak 945.3 ng/mL), respectively. Conclusions: Ace-K and sucralose transfer into breast milk following ingestion of a diet soda. Future research should measure concentrations after repeated exposure and determine whether chronic ingestion of sucralose and Acesulfame-Potassium via the breast milk has clinically relevant health consequences.

  • plasma concentrations of sucralose in children and adults
    Toxicological & Environmental Chemistry, 2017
    Co-Authors: Allison C Sylvetsky, Viviana Bauman, Jenny E Blau, Martin H Garraffo, Peter Walter, Kristina I Rother
    Abstract:

    ABSTRACTWe aimed to measure concentrations of the commonly used artificial sweetener sucralose, following ingestion of doses reflecting a range of consumption and to compare concentrations in children and adults. Eleven adults consumed 355 mL water containing 0 mg (control), 68, 170, or 250 mg sucralose (equivalent to 1–4 diet sodas). A second group of adults (n = 11) consumed 355 mL Diet Rite Cola™ (68 mg sucralose and 41 mg Acesulfame-Potassium (ace-K)) or 68 mg sucralose and 41 mg ace-K in seltzer. Beverages were provided at separate visits in randomized order, prior to an oral glucose tolerance test. Eleven children consumed 0 or 68 mg sucralose in 240 mL water, in an identical study design. Blood was collected before beverage ingestion and serially for 120 min. Sucralose doses (corrected for weight) resulted in similar plasma concentrations in children and adults. Concentrations were comparable whether sucralose was administered in water, combined with ace-K, or in diet soda. Due to their lower body ...

  • plasma concentrations of sucralose in children and adults
    Toxicological & Environmental Chemistry, 2017
    Co-Authors: Allison C Sylvetsky, Viviana Bauman, Jenny E Blau, Martin H Garraffo, Peter Walter, Kristina I Rother
    Abstract:

    ABSTRACTWe aimed to measure concentrations of the commonly used artificial sweetener sucralose, following ingestion of doses reflecting a range of consumption and to compare concentrations in children and adults. Eleven adults consumed 355 mL water containing 0 mg (control), 68, 170, or 250 mg sucralose (equivalent to 1–4 diet sodas). A second group of adults (n = 11) consumed 355 mL Diet Rite Cola™ (68 mg sucralose and 41 mg Acesulfame-Potassium (ace-K)) or 68 mg sucralose and 41 mg ace-K in seltzer. Beverages were provided at separate visits in randomized order, prior to an oral glucose tolerance test. Eleven children consumed 0 or 68 mg sucralose in 240 mL water, in an identical study design. Blood was collected before beverage ingestion and serially for 120 min. Sucralose doses (corrected for weight) resulted in similar plasma concentrations in children and adults. Concentrations were comparable whether sucralose was administered in water, combined with ace-K, or in diet soda. Due to their lower body ...