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Feeding butter with elevated content of trans-10, cis-12 conjugated linoleic acid to obese-prone rats impairs glucose and insulin tolerance.

Hamilton M, Hopkins LE, AlZahal O, MacDonald TL, Cervone DT, Wright DC, McBride BW, Dyck DJ - Lipids Health Dis (2015)

Bottom Line: We recently demonstrated that feeding a natural CLAt10,c12-enriched butter to lean female rats resulted in small, but significant increases in fasting glucose and insulin concentrations, and impaired insulin tolerance.Increasing the consumption of a food naturally enriched with CLAt10,c12 significantly worsens glucose and insulin tolerance in a diabetes-prone rodent model.This outcome is not explained by changes in tissue insulin signaling, physical activity, energy expenditure, food intake or body mass.

View Article: PubMed Central - PubMed

Affiliation: Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, N1G2W1, Canada.

ABSTRACT

Background: We recently demonstrated that feeding a natural CLAt10,c12-enriched butter to lean female rats resulted in small, but significant increases in fasting glucose and insulin concentrations, and impaired insulin tolerance. Our goal was to extend these findings by utilizing the diabetes-prone female fatty Zucker rat. Rats were fed custom diets containing 45 % kcal of fat derived from control and CLAt10,c12-enriched butter for 8 weeks.

Methods: CLA t10,c12-enriched butter was prepared from milk collected from cows fed a high fermentable carbohydrate diet to create subacute rumen acidosis (SARA); control (non-SARA) butter was collected from cows fed a low grain diet. Female fatty Zucker rats (10 weeks old) were randomly assigned to one of four diet treatments: i) low fat (10 % kcal), ii) 45 % kcal lard, iii) 45 % kcal SARA butter, or iv) 45 % kcal non-SARA butter. A low fat fed lean Zucker group was used as a control group. After 8 weeks, i) glucose and insulin tolerance tests, ii) insulin signaling in muscle, adipose and liver, and iii) metabolic caging measurements were performed.

Results: Glucose and insulin tolerance were significantly impaired in all fatty Zucker groups, but to the greatest extent in the LARD and SARA conditions. Insulin signaling (AKT phosphorylation) was impaired in muscle, visceral (perigonadal) adipose tissue and liver in fatty Zucker rats, but was generally similar across dietary groups. Physical activity, oxygen consumption, food intake and weight gain were also similar amongst the various fatty Zucker groups.

Conclusions: Increasing the consumption of a food naturally enriched with CLAt10,c12 significantly worsens glucose and insulin tolerance in a diabetes-prone rodent model. This outcome is not explained by changes in tissue insulin signaling, physical activity, energy expenditure, food intake or body mass.

No MeSH data available.


Related in: MedlinePlus

Phosphorylated Thr and Ser AKT content in subcutaneous (a, b) and visceral (c, d) adipose tissue before and after an acute insulin injection. Data are presented as mean plus standard error. n = 8−10 per group. Groups which share a letter are not statistically different. * indicates a significant difference between pre and post insulin conditions. Statistical significance accepted at p < 0.05. LZ, lean Zuckers; FZ, fatty Zuckers; LF, low fat; SARA, subacute rumen acidosis
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Fig3: Phosphorylated Thr and Ser AKT content in subcutaneous (a, b) and visceral (c, d) adipose tissue before and after an acute insulin injection. Data are presented as mean plus standard error. n = 8−10 per group. Groups which share a letter are not statistically different. * indicates a significant difference between pre and post insulin conditions. Statistical significance accepted at p < 0.05. LZ, lean Zuckers; FZ, fatty Zuckers; LF, low fat; SARA, subacute rumen acidosis

Mentions: In SQAT (Fig. 3), insulin administration significantly increased p-Ser AKT in lean Zuckers, LF and SARA fatty Zuckers, but not in the LARD and non-SARA groups (p < 0.05). p-Thr AKT was increased in all groups, and was the greatest in the lean Zuckers and the least in the low-fat fed fatty Zuckers (p < 0.05). In VAT (Fig. 3), insulin response was consistently impaired in the high fat fed fatty Zucker rats. Insulin acutely increased p-Ser AKT in lean and non-SARA Zuckers (p < 0.05), although the response was significantly blunted in the non-SARA group. p-Thr AKT increased in response to insulin only in the low-fat fed lean and fatty Zuckers (p < 0.05), but not the Lard, SARA or non-SARA groups.Fig. 3


Feeding butter with elevated content of trans-10, cis-12 conjugated linoleic acid to obese-prone rats impairs glucose and insulin tolerance.

Hamilton M, Hopkins LE, AlZahal O, MacDonald TL, Cervone DT, Wright DC, McBride BW, Dyck DJ - Lipids Health Dis (2015)

Phosphorylated Thr and Ser AKT content in subcutaneous (a, b) and visceral (c, d) adipose tissue before and after an acute insulin injection. Data are presented as mean plus standard error. n = 8−10 per group. Groups which share a letter are not statistically different. * indicates a significant difference between pre and post insulin conditions. Statistical significance accepted at p < 0.05. LZ, lean Zuckers; FZ, fatty Zuckers; LF, low fat; SARA, subacute rumen acidosis
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4587826&req=5

Fig3: Phosphorylated Thr and Ser AKT content in subcutaneous (a, b) and visceral (c, d) adipose tissue before and after an acute insulin injection. Data are presented as mean plus standard error. n = 8−10 per group. Groups which share a letter are not statistically different. * indicates a significant difference between pre and post insulin conditions. Statistical significance accepted at p < 0.05. LZ, lean Zuckers; FZ, fatty Zuckers; LF, low fat; SARA, subacute rumen acidosis
Mentions: In SQAT (Fig. 3), insulin administration significantly increased p-Ser AKT in lean Zuckers, LF and SARA fatty Zuckers, but not in the LARD and non-SARA groups (p < 0.05). p-Thr AKT was increased in all groups, and was the greatest in the lean Zuckers and the least in the low-fat fed fatty Zuckers (p < 0.05). In VAT (Fig. 3), insulin response was consistently impaired in the high fat fed fatty Zucker rats. Insulin acutely increased p-Ser AKT in lean and non-SARA Zuckers (p < 0.05), although the response was significantly blunted in the non-SARA group. p-Thr AKT increased in response to insulin only in the low-fat fed lean and fatty Zuckers (p < 0.05), but not the Lard, SARA or non-SARA groups.Fig. 3

Bottom Line: We recently demonstrated that feeding a natural CLAt10,c12-enriched butter to lean female rats resulted in small, but significant increases in fasting glucose and insulin concentrations, and impaired insulin tolerance.Increasing the consumption of a food naturally enriched with CLAt10,c12 significantly worsens glucose and insulin tolerance in a diabetes-prone rodent model.This outcome is not explained by changes in tissue insulin signaling, physical activity, energy expenditure, food intake or body mass.

View Article: PubMed Central - PubMed

Affiliation: Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, N1G2W1, Canada.

ABSTRACT

Background: We recently demonstrated that feeding a natural CLAt10,c12-enriched butter to lean female rats resulted in small, but significant increases in fasting glucose and insulin concentrations, and impaired insulin tolerance. Our goal was to extend these findings by utilizing the diabetes-prone female fatty Zucker rat. Rats were fed custom diets containing 45 % kcal of fat derived from control and CLAt10,c12-enriched butter for 8 weeks.

Methods: CLA t10,c12-enriched butter was prepared from milk collected from cows fed a high fermentable carbohydrate diet to create subacute rumen acidosis (SARA); control (non-SARA) butter was collected from cows fed a low grain diet. Female fatty Zucker rats (10 weeks old) were randomly assigned to one of four diet treatments: i) low fat (10 % kcal), ii) 45 % kcal lard, iii) 45 % kcal SARA butter, or iv) 45 % kcal non-SARA butter. A low fat fed lean Zucker group was used as a control group. After 8 weeks, i) glucose and insulin tolerance tests, ii) insulin signaling in muscle, adipose and liver, and iii) metabolic caging measurements were performed.

Results: Glucose and insulin tolerance were significantly impaired in all fatty Zucker groups, but to the greatest extent in the LARD and SARA conditions. Insulin signaling (AKT phosphorylation) was impaired in muscle, visceral (perigonadal) adipose tissue and liver in fatty Zucker rats, but was generally similar across dietary groups. Physical activity, oxygen consumption, food intake and weight gain were also similar amongst the various fatty Zucker groups.

Conclusions: Increasing the consumption of a food naturally enriched with CLAt10,c12 significantly worsens glucose and insulin tolerance in a diabetes-prone rodent model. This outcome is not explained by changes in tissue insulin signaling, physical activity, energy expenditure, food intake or body mass.

No MeSH data available.


Related in: MedlinePlus