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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) Total body fat as measured by noninvasive echoMRI. Body fat was measured every 6 weeks after the start of treatment. (B) Weights of epidydmal, visceral, and total fat of different groups obtained at the end of the experiment protocol. (C) Lean body mass as a percentage of total body weight measured at 30 weeks of treatment. *= P < 0.05 as compared to other groups.
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f0002: (A) Total body fat as measured by noninvasive echoMRI. Body fat was measured every 6 weeks after the start of treatment. (B) Weights of epidydmal, visceral, and total fat of different groups obtained at the end of the experiment protocol. (C) Lean body mass as a percentage of total body weight measured at 30 weeks of treatment. *= P < 0.05 as compared to other groups.

Mentions: Body fat as determined by non-invasive echoMRI was similar in all 3 treatment groups at the start of the study but lower in the control group (Fig. 2A). CORM-A1 treatment resulted in significant decrease in body fat starting at week 18 of the study and was decreased by 66% of control levels by the of the 30 week treatment protocol (Fig. 2A). Fat mass, as determined by the weight of various fat pad depots at the end of the study, was significantly lower in CORM-A1 treated mice versus all other groups (Fig. 2B). CORM-A1 treatment resulted in significant increase in lean body mass as a percent of total body weight at 30 weeks with lean muscle mass increased 45% in CORM-A1 as compared to control, saline, and iCORM-A1 treated mice (Fig. 2C). While CORM-A1 treated mice exhibited a significant increase in the percent lean mass as compared to the other groups, this was due to the significant loss of fat mass and body weight rather than an increase in actual muscle mass in these mice.Figure 2.


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) Total body fat as measured by noninvasive echoMRI. Body fat was measured every 6 weeks after the start of treatment. (B) Weights of epidydmal, visceral, and total fat of different groups obtained at the end of the experiment protocol. (C) Lean body mass as a percentage of total body weight measured at 30 weeks of treatment. *= 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

f0002: (A) Total body fat as measured by noninvasive echoMRI. Body fat was measured every 6 weeks after the start of treatment. (B) Weights of epidydmal, visceral, and total fat of different groups obtained at the end of the experiment protocol. (C) Lean body mass as a percentage of total body weight measured at 30 weeks of treatment. *= P < 0.05 as compared to other groups.
Mentions: Body fat as determined by non-invasive echoMRI was similar in all 3 treatment groups at the start of the study but lower in the control group (Fig. 2A). CORM-A1 treatment resulted in significant decrease in body fat starting at week 18 of the study and was decreased by 66% of control levels by the of the 30 week treatment protocol (Fig. 2A). Fat mass, as determined by the weight of various fat pad depots at the end of the study, was significantly lower in CORM-A1 treated mice versus all other groups (Fig. 2B). CORM-A1 treatment resulted in significant increase in lean body mass as a percent of total body weight at 30 weeks with lean muscle mass increased 45% in CORM-A1 as compared to control, saline, and iCORM-A1 treated mice (Fig. 2C). While CORM-A1 treated mice exhibited a significant increase in the percent lean mass as compared to the other groups, this was due to the significant loss of fat mass and body weight rather than an increase in actual muscle mass in these mice.Figure 2.

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