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Study · Animal study (in vivo) · mouse · 2006

15 results

AICAR inhibits adipocyte differentiation in 3T3L1 and restores metabolic alterations in diet-induced obesity mice model.

Giri S, Rattan R, Haq E, Khan M, Yasmin R, Won JS, Key L, Singh AK, Singh I

Nutrition & metabolism10 Aug 2006Cited by 143 (Europe PMC)

Summary

BackgroundObesity is one of the principal causative factors involved in the development of metabolic syndrome. AMP-activated protein kinase (AMPK) is an energy sensor that regulates cellular metabolism. The role of AMP-activated protein kinase in adipocyte differentiation is not completely understood, therefore, we examined the effect of 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR), a pharmacological activator of AMP-activated protein kinase (AMPK) on adipocyte differentiation in 3T3L1 cells and in a mouse Diet induced obesity (DIO) model.MethodsTo examine the effect of AICAR on adipocyte differentiation in 3T3L1 cells and in a mouse Diet induced obesity (DIO) model, 3T3L1 cells were differentiated in the presence or absence of different concentration of AICAR and neutral lipid content and expression of various adipocyte-specific transcription factors were examined. In vivo study, treated and untreated mice with AICAR (0.1-0.5 mg/g body weight) were fed high-fat diet (60% kcal% fat) to induce DIO and several parameters were studied.ResultsAICAR blocked adipogenic conversion in 3T3L1 cells along with significant decrease in the neutral lipid content by downregulating several adipocyte-specific transcription factors including peroxisome proliferators-activated receptor gamma (PPARgamma), C/EBPalpha and ADD1/SREBP1, which are critical for adipogenesis in vitro. Moreover, intraperitoneal administration of AICAR (0.5 mg g/body weight) to mice fed with high-fat diet (60% kcal% fat) to induce DIO, significantly blocked the body weight gain and total content of epididymal fat in these mice over a period of 6 weeks. AICAR treatment also restored normal adipokine levels and resulted in significant improvement in glucose tolerance and insulin sensitivity. The reduction in adipose tissue content in AICAR treated DIO mice was due to reduction in lipid accumulation in the pre-existing adipocytes. However, no change was observed in the expression of PPARgamma, C/EBPalpha and ADD1/SREBP1 transcription factors in vivo though PGC1alpha expression was significantly induced.ConclusionThis study suggests that AICAR inhibits adipocyte differentiation via downregulation of expression of adipogenic factors in vitro and reduces adipose tissue content in DIO mice by activating expression of PGC1alpha without inhibiting adipocyte-specific transcription factors in DIO mice.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study15

15 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In high-fat-fed mice, AICAR significantly blocked body weight gain.

    In plain wordsIn mice fed a high-fat diet, AICAR reduced weight gain compared with untreated mice.

    Outcome
    DecreaseBody weight gain
    Study

    mousen: not reported in source

    diet-induced obesity
    Comparator
    untreated mice
    Outcome group
    Body weight · Metabolic and weight
    Studied dose
    0.5 mg g/body weight · intraperitoneal · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Moreover, intraperitoneal administration of AICAR (0.5 mg g/body weight) to mice fed with high-fat diet (60% kcal% fat) to induce DIO, significantly blocked the body weight gain and total content of epididymal fat in these mice over a period of 6 weeks.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In high-fat-fed mice, AICAR significantly reduced total epididymal fat content.

    In plain wordsIn mice fed a high-fat diet, AICAR reduced epididymal fat compared with untreated mice.

    Outcome
    DecreaseEpididymal fat content
    Study

    mousen: not reported in source

    diet-induced obesity
    Comparator
    untreated mice
    Outcome group
    Body composition · Metabolic and weight
    Studied dose
    0.5 mg g/body weight · intraperitoneal · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Moreover, intraperitoneal administration of AICAR (0.5 mg g/body weight) to mice fed with high-fat diet (60% kcal% fat) to induce DIO, significantly blocked the body weight gain and total content of epididymal fat in these mice over a period of 6 weeks.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In diet-induced obese mice, AICAR restored normal adipokine levels.

    In plain wordsIn obese mice, AICAR restored normal fat tissue hormone levels compared with untreated mice.

    Outcome
    Direction not reportedAdipokine levels
    Study

    mousen: not reported in source

    diet-induced obesity
    Comparator
    untreated mice
    Outcome group
    Adipokines · Metabolic and weight
    Studied dose
    0.5 mg g/body weight · intraperitoneal · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    AICAR treatment also restored normal adipokine levels and resulted in significant improvement in glucose tolerance and insulin sensitivity.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In diet-induced obese mice, AICAR significantly improved glucose tolerance.

    In plain wordsIn obese mice, AICAR improved glucose tolerance compared with untreated mice.

    Outcome
    IncreaseGlucose tolerance
    Study

    mousen: not reported in source

    diet-induced obesity
    Comparator
    untreated mice
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    0.5 mg g/body weight · intraperitoneal · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    AICAR treatment also restored normal adipokine levels and resulted in significant improvement in glucose tolerance and insulin sensitivity.
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In diet-induced obese mice, AICAR significantly improved insulin sensitivity.

    In plain wordsIn obese mice, AICAR improved insulin sensitivity compared with untreated mice.

    Outcome
    IncreaseInsulin sensitivity
    Study

    mousen: not reported in source

    diet-induced obesity
    Comparator
    untreated mice
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    0.5 mg g/body weight · intraperitoneal · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    AICAR treatment also restored normal adipokine levels and resulted in significant improvement in glucose tolerance and insulin sensitivity.
  6. 06AnimalAnimal study (in vivo)Efficacy outcome

    In diet-induced obese mice, AICAR reduced lipid accumulation in existing adipocytes.

    In plain wordsIn obese mice, AICAR reduced fat accumulation in existing fat cells compared with untreated mice.

    Outcome
    DecreaseLipid accumulation in existing adipocytes
    Study

    mousen: not reported in source

    diet-induced obesity
    Comparator
    untreated mice
    Outcome group
    Lipids · Metabolic and weight
    Studied dose
    0.5 mg g/body weight · intraperitoneal · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    The reduction in adipose tissue content in AICAR treated DIO mice was due to reduction in lipid accumulation in the pre-existing adipocytes.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In diet-induced obese mice, AICAR did not change PPARgamma expression.

    In plain wordsIn obese mice, AICAR did not change PPARgamma expression compared with untreated mice.

    Outcome
    No significant changePPARgamma expression in vivo
    Study

    mousen: not reported in source

    diet-induced obesity
    Comparator
    untreated mice
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    0.5 mg g/body weight · intraperitoneal · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    However, no change was observed in the expression of PPARgamma, C/EBPalpha and ADD1/SREBP1 transcription factors in vivo though PGC1alpha expression was significantly induced.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In diet-induced obese mice, AICAR did not change C/EBPalpha expression.

    In plain wordsIn obese mice, AICAR did not change C/EBPalpha expression compared with untreated mice.

    Outcome
    No significant changeC/EBPalpha expression in vivo
    Study

    mousen: not reported in source

    diet-induced obesity
    Comparator
    untreated mice
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    0.5 mg g/body weight · intraperitoneal · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    However, no change was observed in the expression of PPARgamma, C/EBPalpha and ADD1/SREBP1 transcription factors in vivo though PGC1alpha expression was significantly induced.
  9. 09AnimalAnimal study (in vivo)Mechanism

    In diet-induced obese mice, AICAR did not change ADD1/SREBP1 expression.

    In plain wordsIn obese mice, AICAR did not change ADD1/SREBP1 expression compared with untreated mice.

    Outcome
    No significant changeADD1/SREBP1 expression in vivo
    Study

    mousen: not reported in source

    diet-induced obesity
    Comparator
    untreated mice
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    0.5 mg g/body weight · intraperitoneal · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    However, no change was observed in the expression of PPARgamma, C/EBPalpha and ADD1/SREBP1 transcription factors in vivo though PGC1alpha expression was significantly induced.
  10. 10AnimalAnimal study (in vivo)Mechanism

    In diet-induced obese mice, AICAR significantly induced PGC1alpha expression.

    In plain wordsIn obese mice, AICAR increased PGC1alpha expression compared with untreated mice.

    Outcome
    IncreasePGC1alpha expression in vivo
    Study

    mousen: not reported in source

    diet-induced obesity
    Comparator
    untreated mice
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    0.5 mg g/body weight · intraperitoneal · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    However, no change was observed in the expression of PPARgamma, C/EBPalpha and ADD1/SREBP1 transcription factors in vivo though PGC1alpha expression was significantly induced.
  11. 11LabIn vitro (cells)Efficacy outcome

    In 3T3L1 cells, AICAR blocked adipogenic conversion versus absence of AICAR.

    In plain wordsIn cells, AICAR blocked fat cell development compared with no AICAR.

    Outcome
    DecreaseAdipogenic conversion
    Study

    n: not reported in source

    3T3L1 cells
    Comparator
    absence of AICAR
    Outcome group
    Body composition · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR blocked adipogenic conversion in 3T3L1 cells along with significant decrease in the neutral lipid content
    1 context sentence
    Summary · context
    To examine the effect of AICAR on adipocyte differentiation in 3T3L1 cells and in a mouse Diet induced obesity (DIO) model, 3T3L1 cells were differentiated in the presence or absence of different concentration of AICAR and neutral lipid content and expression of various adipocyte-specific transcription factors were examined.
  12. 12LabIn vitro (cells)Efficacy outcome

    In 3T3L1 cells, AICAR significantly decreased neutral lipid content versus absence of AICAR.

    In plain wordsIn cells, AICAR reduced neutral fat content compared with no AICAR.

    Outcome
    DecreaseNeutral lipid content
    Study

    n: not reported in source

    3T3L1 cells
    Comparator
    absence of AICAR
    Outcome group
    Lipids · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR blocked adipogenic conversion in 3T3L1 cells along with significant decrease in the neutral lipid content
    1 context sentence
    Summary · context
    To examine the effect of AICAR on adipocyte differentiation in 3T3L1 cells and in a mouse Diet induced obesity (DIO) model, 3T3L1 cells were differentiated in the presence or absence of different concentration of AICAR and neutral lipid content and expression of various adipocyte-specific transcription factors were examined.
  13. 13LabIn vitro (cells)Mechanism

    In 3T3L1 cells, AICAR downregulated PPARgamma expression.

    In plain wordsIn cells, AICAR reduced PPARgamma expression compared with no AICAR.

    Outcome
    DecreasePPARgamma expression
    Study

    n: not reported in source

    3T3L1 cells
    Comparator
    absence of AICAR
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    by downregulating several adipocyte-specific transcription factors including peroxisome proliferators-activated receptor gamma (PPARgamma), C/EBPalpha and ADD1/SREBP1, which are critical for adipogenesis in vitro.
    1 context sentence
    Summary · context
    To examine the effect of AICAR on adipocyte differentiation in 3T3L1 cells and in a mouse Diet induced obesity (DIO) model, 3T3L1 cells were differentiated in the presence or absence of different concentration of AICAR and neutral lipid content and expression of various adipocyte-specific transcription factors were examined.
  14. 14LabIn vitro (cells)Mechanism

    In 3T3L1 cells, AICAR downregulated C/EBPalpha expression.

    In plain wordsIn cells, AICAR reduced C/EBPalpha expression compared with no AICAR.

    Outcome
    DecreaseC/EBPalpha expression
    Study

    n: not reported in source

    3T3L1 cells
    Comparator
    absence of AICAR
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    by downregulating several adipocyte-specific transcription factors including peroxisome proliferators-activated receptor gamma (PPARgamma), C/EBPalpha and ADD1/SREBP1, which are critical for adipogenesis in vitro.
    1 context sentence
    Summary · context
    To examine the effect of AICAR on adipocyte differentiation in 3T3L1 cells and in a mouse Diet induced obesity (DIO) model, 3T3L1 cells were differentiated in the presence or absence of different concentration of AICAR and neutral lipid content and expression of various adipocyte-specific transcription factors were examined.
  15. 15LabIn vitro (cells)Mechanism

    In 3T3L1 cells, AICAR downregulated ADD1/SREBP1 expression.

    In plain wordsIn cells, AICAR reduced ADD1/SREBP1 expression compared with no AICAR.

    Outcome
    DecreaseADD1/SREBP1 expression
    Study

    n: not reported in source

    3T3L1 cells
    Comparator
    absence of AICAR
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    by downregulating several adipocyte-specific transcription factors including peroxisome proliferators-activated receptor gamma (PPARgamma), C/EBPalpha and ADD1/SREBP1, which are critical for adipogenesis in vitro.
    1 context sentence
    Summary · context
    To examine the effect of AICAR on adipocyte differentiation in 3T3L1 cells and in a mouse Diet induced obesity (DIO) model, 3T3L1 cells were differentiated in the presence or absence of different concentration of AICAR and neutral lipid content and expression of various adipocyte-specific transcription factors were examined.

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Version history

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  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

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