Limits...
Chronic treatment with a carbon monoxide releasing molecule reverses dietary induced obesity in mice.

Hosick PA, AlAmodi AA, Hankins MW, Stec DE - Adipocyte (2015)

Bottom Line: Chronic treatment with CORM-A1 resulted in a 33% decrease from initial body weight over the 30 week treatment period while treatment with iCORM and saline were associated with 18 and 25% gain in initial body weight over the same time frame.Chronic treatment with CORM-A1 did not affect food intake or activity but resulted in a significant increase in metabolism.CORM-A1 treatment also resulted in lower fasting blood glucose, improvement in insulin sensitivity and decreased heptatic steatosis.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology & Biophysics; Center for Excellence in Cardiovascular-Renal Research; University of Mississippi Medical Center; Jackson, MS USA; Department of Exercise Science and Physical Education; Montclair State University; Montclair, NJ USA.

ABSTRACT
Chronic, low level treatment with a carbon monoxide releasing molecule (CO-RM), CORM-A1, has been shown to prevent the development of obesity in response to a high fat diet. The objective of this study was to test the hypothesis that chronic, low level treatment with this CO-RM can reverse established obesity via a mechanism independent of food intake. Dietary induced obese mice were treated with CORM-A1, the inactive compound iCORM-A1, or saline every 48 hours for 30 weeks while maintained on a high fat (60%) diet. Chronic treatment with CORM-A1 resulted in a 33% decrease from initial body weight over the 30 week treatment period while treatment with iCORM and saline were associated with 18 and 25% gain in initial body weight over the same time frame. Chronic treatment with CORM-A1 did not affect food intake or activity but resulted in a significant increase in metabolism. CORM-A1 treatment also resulted in lower fasting blood glucose, improvement in insulin sensitivity and decreased heptatic steatosis. Chronic treatment with CO releasing molecules can reverse dietary induced obesity and normalize insulin resistance independent of changes in food intake or activity. These findings are likely though a mechanism which increases metabolism.

No MeSH data available.


Related in: MedlinePlus

Representative Western blots from epidydmal fat tissues from control, saline treated, iCORM-A1 and CORM-A1 treated mice (n = 6). (A) Representative blots. (B) Levels of PGC1-α. (C) Levels of NRF1. (D) Levels of UCP1. (E) Levels of HMGB1. * = significant from control mice, P < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4836479&req=5

f0005: Representative Western blots from epidydmal fat tissues from control, saline treated, iCORM-A1 and CORM-A1 treated mice (n = 6). (A) Representative blots. (B) Levels of PGC1-α. (C) Levels of NRF1. (D) Levels of UCP1. (E) Levels of HMGB1. * = significant from control mice, P < 0.05.

Mentions: In samples of epidydimal fat, chronic CORM-A1 treatment increased levels of peroxisomal proliferating activating receptor- γ coactivator (PGC-1α) and nuclear respiratory factor-1 (NRF-1) which are considered markers of mitochondrial biogenesis (Fig. 5A, B, C). Levels of uncoupling protein-1 (UCP1) were also increased in epidydimal fat of CORM-A1 treated mice (Fig. 5A and D). Obesity is associated with elevated levels of inflammation. We examined the protein levels of high mobility group box-1 (HMGB1) in the epidydmal fat in each of the groups to determine the effect of chronic CORM-A1 treatment on HMGB1 in white adipose tissue. CORM-A1 treatment significantly attenuated HMGB1 levels in dietary-induced obese mice as compared to all other groups (Fig. 5A and E).Figure 5.


Chronic treatment with a carbon monoxide releasing molecule reverses dietary induced obesity in mice.

Hosick PA, AlAmodi AA, Hankins MW, Stec DE - Adipocyte (2015)

Representative Western blots from epidydmal fat tissues from control, saline treated, iCORM-A1 and CORM-A1 treated mice (n = 6). (A) Representative blots. (B) Levels of PGC1-α. (C) Levels of NRF1. (D) Levels of UCP1. (E) Levels of HMGB1. * = significant from control mice, P < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4836479&req=5

f0005: Representative Western blots from epidydmal fat tissues from control, saline treated, iCORM-A1 and CORM-A1 treated mice (n = 6). (A) Representative blots. (B) Levels of PGC1-α. (C) Levels of NRF1. (D) Levels of UCP1. (E) Levels of HMGB1. * = significant from control mice, P < 0.05.
Mentions: In samples of epidydimal fat, chronic CORM-A1 treatment increased levels of peroxisomal proliferating activating receptor- γ coactivator (PGC-1α) and nuclear respiratory factor-1 (NRF-1) which are considered markers of mitochondrial biogenesis (Fig. 5A, B, C). Levels of uncoupling protein-1 (UCP1) were also increased in epidydimal fat of CORM-A1 treated mice (Fig. 5A and D). Obesity is associated with elevated levels of inflammation. We examined the protein levels of high mobility group box-1 (HMGB1) in the epidydmal fat in each of the groups to determine the effect of chronic CORM-A1 treatment on HMGB1 in white adipose tissue. CORM-A1 treatment significantly attenuated HMGB1 levels in dietary-induced obese mice as compared to all other groups (Fig. 5A and E).Figure 5.

Bottom Line: Chronic treatment with CORM-A1 resulted in a 33% decrease from initial body weight over the 30 week treatment period while treatment with iCORM and saline were associated with 18 and 25% gain in initial body weight over the same time frame.Chronic treatment with CORM-A1 did not affect food intake or activity but resulted in a significant increase in metabolism.CORM-A1 treatment also resulted in lower fasting blood glucose, improvement in insulin sensitivity and decreased heptatic steatosis.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology & Biophysics; Center for Excellence in Cardiovascular-Renal Research; University of Mississippi Medical Center; Jackson, MS USA; Department of Exercise Science and Physical Education; Montclair State University; Montclair, NJ USA.

ABSTRACT
Chronic, low level treatment with a carbon monoxide releasing molecule (CO-RM), CORM-A1, has been shown to prevent the development of obesity in response to a high fat diet. The objective of this study was to test the hypothesis that chronic, low level treatment with this CO-RM can reverse established obesity via a mechanism independent of food intake. Dietary induced obese mice were treated with CORM-A1, the inactive compound iCORM-A1, or saline every 48 hours for 30 weeks while maintained on a high fat (60%) diet. Chronic treatment with CORM-A1 resulted in a 33% decrease from initial body weight over the 30 week treatment period while treatment with iCORM and saline were associated with 18 and 25% gain in initial body weight over the same time frame. Chronic treatment with CORM-A1 did not affect food intake or activity but resulted in a significant increase in metabolism. CORM-A1 treatment also resulted in lower fasting blood glucose, improvement in insulin sensitivity and decreased heptatic steatosis. Chronic treatment with CO releasing molecules can reverse dietary induced obesity and normalize insulin resistance independent of changes in food intake or activity. These findings are likely though a mechanism which increases metabolism.

No MeSH data available.


Related in: MedlinePlus