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Cited by 14Natural Antidiabetic Agents StudiesMetabolism, Diabetes, and CancerAdipokines, Inflammation, and Metabolic Diseases

Hypoglycemic effects of brassinosteroid in diet-induced obese mice

Open access
Esposito, Debora, Kizelsztein, Pablo, Komarnytsky, Slavko, Raskin, Ilya·2012·American Journal of Physiology-Endocrinology and Metabolism
DOI 10.1152/ajpendo.00024.2012PMC PMC3774328
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Abstract

The prevalence of obesity is increasing globally, and obesity is a major risk factor for metabolic diseases such as type 2 diabetes. Previously, we reported that oral administration of homobrassinolide (HB) to healthy rats triggered a selective anabolic response that was associated with lower blood glucose. Therefore, the aim of this study was to evaluate the effects of HB administration on glucose metabolism, insulin sensitivity, body composition, and gluconeogenic gene expression profiles in liver of C57BL/6J high-fat diet-induced obese mice. Acute oral administration of 50–300 mg/kg HB to obese mice resulted in a dose-dependent decrease in fasting blood glucose within 3 h of treatment. Daily chronic administration of HB (50 mg/kg for 8 wk) ameliorated hyperglycemia and improved oral glucose tolerance associated with obesity without significantly affecting body weight or body composition. These changes were accompanied by lower expression of two key gluconeogenic enzymes, phospho enolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G-6-Pase), and increased phosphorylation of AMP-activated protein kinase in the liver and muscle tissue. In vitro, HB treatment (1–15 μM) inhibited cyclic AMP-stimulated but not dexamethasone-stimulated upregulation of PEPCK and G-6-Pase mRNA levels in H4IIE rat hepatoma cells. Among a series of brassinosteroid analogs related to HB, only homocastasterone decreased glucose production in cell culture significantly. These results indicate the antidiabetic effects of brassinosteroids and begin to elucidate their putative cellular targets both in vitro and in vivo.

AI snapshot

Written from the paper’s full text.

TL;DR

Oral homobrassinolide (HB) lowered fasting blood glucose acutely and improved oral glucose tolerance chronically in diet-induced obese C57BL/6J mice without changing body weight or body composition. These effects were accompanied by reduced hepatic PEPCK and G-6-Pase expression and increased AMPK/Akt signaling, with in vitro evidence that HB suppresses cAMP-induced gluconeogenic gene expression.

Key findings

  • Acute oral HB (50–300 mg/kg) caused a dose-dependent decrease in fasting blood glucose within 3 h; at 300 mg/kg the effect reached about one-half of that observed with metformin.
  • Chronic HB (50 mg/kg daily for 8 wk) improved oral glucose tolerance: blood glucose was significantly lower at 60 and 120 min after glucose challenge, and total AUC decreased by an average of 18%; final body weight, lean/fat mass, bone mineral content, and food intake did not differ significantly. Final baseline glucose was not significantly different between groups (229 ± 17 mg/dl), but HB-treated animals had lower glucose after acute HB several days before study end.
  • HB reduced liver mRNA for PEPCK and G-6-Pase two- and threefold, respectively, increased AMPK phosphorylation in liver and muscle, and increased Akt1/Akt2 phosphorylation in liver plus IRS-1 and Akt1 phosphorylation and total PI3K in muscle.
  • In H4IIE rat hepatoma cells, HB (1–15 μM) inhibited cAMP-stimulated but not dexamethasone-stimulated upregulation of PEPCK and G-6-Pase; among eight brassinosteroid analogs, only homocastasterone significantly decreased glucose production. HB weakly suppressed glucose production (20%) from Dex-cAMP-induced cells but strongly decreased cAMP-induced PEPCK (≤70%) and G-6-Pase (85%) mRNA; insulin 10 nM decreased glucose production by 50%, PEPCK mRNA by 80%, and totally suppressed G-6-Pase transcript.

Methods

  • Male C57BL/6J mice were fed a high-fat diet (60% fat-derived calories) for 4 wk, randomized, maintained on HFD for an additional 6 wk, then gavaged daily with vehicle (n = 8) or HB 50 mg/kg (n = 8) for 8 wk; acute HB doses of 50–300 mg/kg were also tested. Outcomes included fasting glucose, oral glucose tolerance test, DEXA body composition, plasma/tissue lipids, Western blot, and qPCR.
  • H4IIE rat hepatoma cells were treated with dexamethasone-cAMP or cAMP ± HB (1–15 μM) or insulin 10 nM; PEPCK and G-6-Pase mRNA were measured by qPCR, and glucose production was measured in culture medium.
  • Statistics used means ± SE, two-tailed t-test or one-way ANOVA with P < 0.05, Dunnett’s post hoc test, and two-factor repeated-measures ANOVA for body weight gain and glucose tolerance.

Limitations

  • Stated: oral gavage may induce stress and influence weight gain in chronic feeding studies; an alternative low-stress delivery method such as peanut butter pills may be considered for future chronic obesity/type 2 diabetes studies.
  • Stated: the hypothesis that HB modulates glucose metabolism through combined Akt and AMPK signaling was not tested in the present study and needs further clarification.
  • Evident from text: small group sizes (n = 8), only male C57BL/6J mice, a single chronic HB dose (50 mg/kg), and in vitro work in rat hepatoma cells; no direct in vivo measurement of hepatic glucose production/flux is reported. The paper also notes that the earlier healthy-rat blood glucose reduction was only a trend and that species differences may explain weaker chronic effects in obese mice.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1152/ajpendo.00024.2012

Cites

35 of 35 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 18 cited sources checked · 0 supported · 0 flagged

  • Findingown data
    § RESULTS

    HB treatment increases phosphorylation of AMPK in liver and, to a lesser degree, muscle tissue of diet-induced obese mice.

    “Additionally, Western blot analysis of liver tissue of these animals revealed an increased phosphorylation of AMPK (Fig. 4B), a key regulator of cellular energy homeostasis and suppressor of gluconeogenesis (5). A smaller increase in AMPK phosphorylation was also evident in the muscle tissue of the HB animals (Fig. 4C).”
    Quote in the paperSubstantial claim
  • Findingown data
    § RESULTS

    Chronic daily oral HB at 50 mg/kg for 8 wk improves oral glucose tolerance in high-fat diet-induced obese C57BL/6J mice.

    “an oral glucose tolerance test performed at the end of the study revealed significantly increased insulin sensitivity in HB-treated animals.”
    • Also stated in: § RESULTS · plain
      “The total area under the curve decreased by an average of 18% by treating mice with HB.”
    Quote in the paperSubstantial claim
  • Findingown data
    § RESULTS

    The acute blood glucose-lowering effect of HB at 300 mg/kg is about one-half that of metformin at 300 mg/kg 3 h after oral administration in obese mice.

    “The effect was dose dependent in the range of 50 to 300 mg/kg body wt and reached one-half of that observed for metformin (a standard reference drug used at the highest dose of 300 mg/kg) 3 h after oral administration.”
    Quote in the paperSubstantial claim
  • Findingown data
    § Abstract

    Acute oral administration of homobrassinolide (HB) at 50-300 mg/kg to high-fat diet-induced obese C57BL/6J mice causes a dose-dependent decrease in fasting blood glucose within 3 h.

    “Acute oral administration of 50–300 mg/kg HB to obese mice resulted in a dose-dependent decrease in fasting blood glucose within 3 h of treatment.”
    • Also stated in: § RESULTS · plain
      “HB showed moderate efficacy at lowering blood glucose levels in C57BL/6J mice following the acute single-dose treatment (Fig. 2). The effect was dose dependent in the range of 50 to 300 mg/kg body wt”
    Quote in the paperSubstantial claim
  • Findingown data
    § RESULTS

    HB treatment at 1 or 10 μM for 8 h weakly suppresses glucose production (20%) from Dex-cAMP-induced H4IIE cells.

    “HB treatment (1 or 10 μM for 8 h) achieved weak suppression of glucose production (20%) from Dex-cAMP-induced H4IIE cells in vitro (Fig. 6A).”
    Quote in the paperSubstantial claim
  • May combine two claims. 18
  • The quote only partly states this claim. 1
  • Classified as probably not a substantial claim. 15

  • May combine two claims.

    Findingown data
    § RESULTS

    HB treatment increases insulin-signaling pathway markers in liver and muscle of diet-induced obese mice: Akt1 and Akt2 phosphorylation in liver; IRS-1 and Akt1 phosphorylation and total PI3K in muscle.

    “We observed a significant increase in Akt1 and Akt2 phosphorylation in the liver and a significant increase in IRS-1 and Akt1 phosphorylation in the muscle as well as an increase in total PI3K in muscle tissue.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data
    § RESULTS

    Chronic daily oral HB at 50 mg/kg for 8 wk does not significantly affect body weight, body composition, or food intake in high-fat diet-induced obese C57BL/6J mice.

    “The final body weights did not differ between two groups (Table 1); no changes in food intake (not shown) or body weight gain have also been noted (Fig. 3A). DEXA analysis confirmed these findings by showing no significant changes in either body composition (lean or fat mass) or bone mineral content.”
    Quote in the paperSubstantial claim

  • The quote only partly states this claim.

    Findingown data
    § RESULTS

    Chronic HB treatment at 50 mg/kg for 8 wk reduces hepatic mRNA levels of PEPCK and G-6-Pase in diet-induced obese mice, by about two- and threefold, respectively.

    “In animals treated with HB, the mRNA levels were reduced significantly for PEPCK and G-6-Pase two- and threefold, respectively (Fig. 4A).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data
    § RESULTS

    Among eight brassinosteroid analogs tested, only homocastasterone significantly decreases glucose production in cell culture, similar to HB.

    “Among eight compounds tested, only homocastasterone (2) was able to suppress glucose production from Dex-cAMP-induced cells, similar to HB (Fig. 7).”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S1 (asserted), S3 (load-bearing), S4 (based).

    Findingown data
    § RESULTS

    In H4IIE rat hepatoma cells, HB does not inhibit dexamethasone-stimulated upregulation of PEPCK and G-6-Pase mRNA.

    “A similar weak decrease in PEPCK and G-6-Pase mRNA levels (0–10%) was observed following an induction with a dexamethasone-cAMP mixture (Fig. 6B)”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data
    § RESULTS

    Baseline blood glucose levels continued to rise during the 8-wk treatment and were not significantly different between control and HB-treated groups at the end of treatment (229 ± 17 mg/dl).

    “The baseline blood glucose levels continued to rise for the duration of the treatment and were not significantly different between either group at the end of the treatment (229 ± 17 mg/dl).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingnone given
    § DISCUSSION

    In the present study, both control and treatment groups of mice were obese and showed clear signs of hyperglycemia and insulin resistance.

    “In the present study, both control and treatment groups of mice were obese and showed clear signs of hyperglycemia and insulin resistance.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data
    § RESULTS

    At the beginning of treatment after 10 wk on high-fat diet, all mice had similar weight (33.2 ± 0.9 g) and had developed hyperglycemia (204 ± 11 mg/dl fasting blood glucose).

    “At the beginning of the treatment (after 10 wk on HFD), all animals had similar weight (33.2 ± 0.9 g) and developed hyperglycemia (204 ± 11 mg/dl fasting blood glucose).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationown data
    § Abstract

    These results indicate the antidiabetic effects of brassinosteroids and begin to elucidate their putative cellular targets both in vitro and in vivo.

    “These results indicate the antidiabetic effects of brassinosteroids and begin to elucidate their putative cellular targets both in vitro and in vivo.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning
    § DISCUSSION

    Plant brassinosteroids and ecdysteroids have similar effects on glucose metabolism and insulin sensitivity in animals, but their underlying molecular mechanisms and targets may differ.

    “Taken together, these data suggest that plant brassinosteroids and ecdysteroids have similar effects on glucose metabolism and insulin sensitivity in animals; however, the underlying molecular mechanisms and targets may be different.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationown data
    § DISCUSSION

    Structural features required for plant sterols to modulate carbohydrate metabolism in mammals include 2α- and 3α-hydroxyl groups at C-3 in the A ring, a 6-keto group in the B ring, and 22α,23α-hydroxyls in the side chain.

    “However, it is clear that several structural similarities are required for plant sterols to modulate carbohydrate metabolism in mammals. These include 2a- and 3a-hydroxyl groups at the C-3 position in the A ring, 6-keto group in B ring, and 22a, 23a-hydroxyls in the side chain of the molecule (Fig. 7).”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation
    § RESULTS

    Changes in cAMP concentration are directly involved in transcriptional regulation of PEPCK and G-6-Pase genes through several cis-acting sequences in their promoters.

    “Changes in cAMP concentration are also directly involved in transcriptional regulation of these genes through several cis-acting sequences present in their promoters (8).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [8] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation
    § RESULTS

    PEPCK is highly expressed in the liver, where it is adaptively regulated by hormones and other agents in a manner that parallels gluconeogenic flux.

    “PEPCK is highly expressed in the liver, where it is adaptively regulated by a variety of different hormones and other agents in a manner that parallels gluconeogenic flux (17).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [17] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation
    § RESULTS

    G-6-Pase is expressed mainly in the liver and kidney cortex, particularly in starved and diabetic states.

    “G-6-Pase is expressed mainly in the liver and in the kidney cortex, most particularly in the starved and diabetic states (30).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [30] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation
    § RESULTS

    Glucocorticoids, specifically dexamethasone, cause a larger (≤10-fold) increase in G-6-Pase activity and mRNA in cultured hepatoma cells.

    “Glucocorticoids and specifically dexamethasone cause a larger (≤10-fold) increase in G-6-Pase activity and in the level of its mRNA in cultured hepatoma cells (33).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [33] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation
    § DISCUSSION

    Metformin activates AMPK and inhibits expression of the hepatic gluconeogenic genes PEPCK and G-6-Pase similarly to insulin.

    “Metformin has been shown to activate AMPK and to inhibit the expression of the hepatic gluconeogenic genes PEPCK and G-6-Pase similarly to insulin (19).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [19] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation
    § DISCUSSION

    AMPK regulates IRS-1 and Akt/PKB, whereas insulin and Akt have negative impacts on AMPK activation in adipocytes.

    “It has been reported that AMPK regulates IRS-1 and Akt/PKB (23), whereas insulin and Akt have negative impacts on AMPK activation in adipocytes (6).”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [23] source

      Not checked in the free run.

    • cites [6] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation
    § DISCUSSION

    Metformin reduces hepatic glucose production and improves peripheral insulin sensitivity, thereby ameliorating hyperglycemia.

    “The principal function of metformin is to reduce hepatic glucose production and to improve peripheral insulin sensitivity, thus ameliorating hyperglycemia (20).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [20] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation
    § DISCUSSION

    Activation of AMPK improves insulin sensitivity by stimulating glucose uptake and lowering blood glucose, whereas AMPK activity is suppressed in disorders associated with insulin resistance.

    “The activation of AMPK improves insulin sensitivity by stimulating glucose uptake and lowering blood glucose, whereas the activity of AMPK is suppressed in disorders associated with insulin resistance (31).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [31] source

      Not checked in the free run.

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation
    § Abstract

    20-Hydroxyecdysone decreases weight and hyperglycemia in obese mice.

    “Since another plant ecdysteroid, 20-hydroxyecdysone (20HE), was shown to decrease weight and hypeglycemia in obese mice (21), we sought to explore the effects of HB on glucose metabolism and insulin resistance in the high-fat diet-induced obese C57BL/6J mouse model.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [21] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation
    § RESULTS

    Starvation and diabetes cause a two- to threefold increase in gluconeogenic enzyme activity in the liver associated with a two- to fourfold increase in PEPCK and G-6-Pase mRNA.

    “Starvation and diabetes cause a two- to threefold increase in gluconeogenic enzyme activity in the liver that is associated with a two- to fourfold increase in PEPCK and G-6-Pase mRNA (1).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [1] source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation
    § Abstract

    Oral administration of HB to healthy rats triggers a selective anabolic response associated with lower blood glucose.

    “In our previous study, we observed that oral administration of homobrassinolide (HB; Fig. 1A) to healthy rats triggered a selective anabolic response that was associated with lower blood glucose (11).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [11] source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation
    § Abstract

    C57BL/6J mice were selectively bred for divergent body fat mass and model complex polygenic human obesity.

    “These mice were selectively bred for divergent body fat mass and thus model complex polygenic human obesity (7).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [7] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductown data
    § MATERIALS AND METHODS

    β-actin was used as a loading control in Western blots.

    “and β-actin (Santa Cruz Biotechnology, Santa Cruz, CA) as a loading control according to the manufacturer's instructions.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation
    § DISCUSSION

    Ecdysteroids have a wide array of physiological and pharmacological effects in animals and insects, including modulation of protein synthesis and carbohydrate metabolism.

    “At the same time, brassinosteroids share some similarities with ecdysteroids that have a wide array of physiological and pharmacological effects in animals and insects (4), including modulation of protein synthesis (14) and carbohydrate metabolism (21).”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [4] source

      Not checked in the free run.

    • cites [14] source

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    • cites [21] source

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Study design and conductown data
    § MATERIALS AND METHODS

    Mice were randomized into control and treatment groups.

    “Then animals were further randomized into two groups and fed HFD for an additional 6 wk.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Study design and conductown data
    § RESULTS

    β-actin mRNA level remained unaffected by treatments and was used as an internal standard.

    “whereas the β-actin gene was chosen as an internal standard since the level of β-actin mRNA remained unaffected by the treatments.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation
    § DISCUSSION

    20HE lowers blood glucose in obese mice, causes a significant decrease in body weight gain and adipose mass, and has no effect on food consumption.

    “Previously, we have observed that 20HE, a plant ecdysteroid structurally similar to brassinosteroids, lowered blood glucose in obese mice, whereas it caused a significant decrease in body weight gain and adipose mass. Similarly to HB, 20HE had no effect on food consumption in this model (21).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [21] source

      Not checked in the free run.

28 of 28

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Anabolic, hypoglycaemic and wound-healing effects are associated with brassinosteroids in rodents.

    “since anabolic, hypoglycaemic and wound-healing effects are also associated with brassinosteroids in rodents [213-215]”

    From Ecdysteroids (2021) · cites this paper as [214]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

  • HB group lean and fat masses exceed reported body weight

    Minor

    The HB group's mean lean mass (20.1 g) and fat mass (19.3 g) sum to 39.4 g, but its reported mean body weight is 38.4 g. The control group's corresponding masses sum exactly to its reported body weight.

    Reported 38.4 · recomputed 39.4

1 of 1

Cites

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Research works printed but not linked: 1

  1. Yuan L, 2002, Chin Med J (Engl), 115, 1843

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Related

Authors
Esposito, D., Kizelsztein, P., Komarnytsky, S., & Raskin, I.
Affiliations
  • Biotech Center, School of Environmental and Biological Sciences, Rutgers University, New Brunswick, New Jersey; and
  • Rutgers, The State University of New Jersey (US)
Corresponding author
Komarnytsky, Slavko
ORCID
Venue
American Journal of Physiology-Endocrinology and Metabolism
Publisher
American Physiological Society
Published
2012-09-01
Volume
303
Issue
5
Pages
E652-E658
ISSN
  • 0193-1849 (ISSN-L)
  • 1522-1555
DOI
10.1152/ajpendo.00024.2012
PMC
PMC3774328
OpenAlex
W2126708807
Semantic Scholar
00b2df313abea41d959925bd25700d171e981c03
Cited by
14
References
35
Citations by year
2024: 1 · 2021: 4 · 2020: 1 · 2018: 1 · 2017: 2 · 2016: 1 · 2015: 1 · 2014: 2 · 2013: 1
FWCI
1.03
Type
journal article
Language
en
Open access
Locations
  • American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Center for Complementary and Integrative Health (P50AT002776)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Natural Antidiabetic Agents Studies
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
brassinosteroids, homobrassinolide, diet-induced obesity, hypoglycemic effect, glucose metabolism, insulin sensitivity, oral glucose tolerance, gluconeogenesis, phosphoenolpyruvate carboxykinase, glucose-6-phosphatase, AMPK, liver, muscle, antidiabetic effect, type 2 diabetes
MeSH terms
Cyclic AMP, Animals, Cell Line, Gene Expression Regulation, Glucose-6-Phosphatase, Hyperglycemia, Hypoglycemic Agents, Insulin Resistance, Liver, Male, Mice, Inbred C57BL, Obesity, Phosphorylation, Protein Processing, Post-Translational, Random Allocation, RNA, Messenger, Dietary Supplements, Phosphoenolpyruvate Carboxykinase (ATP), Mice, AMP-Activated Protein Kinases, Diet, High-Fat, Brassinosteroids

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