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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

(A) Daily food intake measured over the first 4 weeks of treatment in each experimental group. (B) Motor activity measured at 28 weeks of treatment in each experimental group. (C) Oxygen consumption measured at 28 weeks of treatment in each experimental group. * = P < 0.05 as compared to other groups.
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f0004: (A) Daily food intake measured over the first 4 weeks of treatment in each experimental group. (B) Motor activity measured at 28 weeks of treatment in each experimental group. (C) Oxygen consumption measured at 28 weeks of treatment in each experimental group. * = P < 0.05 as compared to other groups.

Mentions: In order to determine if CORM-A1 treatment causes weight loss by decreasing food intake, we measure weekly food intake in mice over the first 4 weeks of treatment. Food intake in control, untreated mice was significantly higher as compared with all mice receiving injections over the first 3 weeks of treatment; however, this difference was lost by week 4 of treatment (Fig. 4A). Next, we determined if CORM-A1 treatment increases motor activity to promote weight loss in dietary-induced obese mice. Motor activity was measured in all groups of mice at 28 weeks of treatment. No differences in motor activity were detected between any of the groups (Fig. 4B). Lastly, we measured oxygen consumption as an index of metabolism to determine if CORM-A1 treatment was associated with any alterations in metabolism. CORM-A1 treatment resulted in a doubling of oxygen consumption as compared to all other groups of mice (Fig. 4C).Figure 4.


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

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

(A) Daily food intake measured over the first 4 weeks of treatment in each experimental group. (B) Motor activity measured at 28 weeks of treatment in each experimental group. (C) Oxygen consumption measured at 28 weeks of treatment in each experimental group. * = P < 0.05 as compared to other groups.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f0004: (A) Daily food intake measured over the first 4 weeks of treatment in each experimental group. (B) Motor activity measured at 28 weeks of treatment in each experimental group. (C) Oxygen consumption measured at 28 weeks of treatment in each experimental group. * = P < 0.05 as compared to other groups.
Mentions: In order to determine if CORM-A1 treatment causes weight loss by decreasing food intake, we measure weekly food intake in mice over the first 4 weeks of treatment. Food intake in control, untreated mice was significantly higher as compared with all mice receiving injections over the first 3 weeks of treatment; however, this difference was lost by week 4 of treatment (Fig. 4A). Next, we determined if CORM-A1 treatment increases motor activity to promote weight loss in dietary-induced obese mice. Motor activity was measured in all groups of mice at 28 weeks of treatment. No differences in motor activity were detected between any of the groups (Fig. 4B). Lastly, we measured oxygen consumption as an index of metabolism to determine if CORM-A1 treatment was associated with any alterations in metabolism. CORM-A1 treatment resulted in a doubling of oxygen consumption as compared to all other groups of mice (Fig. 4C).Figure 4.

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