Effects of High-Fat High-Sucrose Feeding, Energy Restriction, andtrans-10,cis-12 Conjugated Linoleic Acid on Visfatin and Apelin in Hamsters

Insulin resistance in the vasculature is a characteristic feature of obesity and contributes to the pathogenesis of vascular dysfunction and disease. However, the molecular mechanisms underlying obesity-associated vascular insulin resistance and dysfunction remain poorly understood. We hypothesized that TRAF3IP2 (TRAF3 interacting protein 2), a proinflammatory adaptor molecule known to activate pathological stress pathways and implicated in cardiovascular diseases, plays a causal role in obesity-associated vascular insulin resistance and dysfunction. We tested this hypothesis by employing genetic-manipulation in endothelial cells in vitro, in isolated arteries ex vivo, and diet-induced obesity in a mouse model of TRAF3IP2 ablation in vivo. We show that ectopic expression of TRAF3IP2 blunts insulin signaling in endothelial cells and diminishes endothelium-dependent vasorelaxation in isolated aortic rings. Further, 16 weeks of high fat/high sucrose feeding impaired glucose tolerance, aortic insulin-induced vasorelaxation, and hindlimb postocclusive reactive hyperemia, while increasing blood pressure and arterial stiffness in wild-type male mice. Notably, TRAF3IP2 ablation protected mice from such high fat/high sucrose feeding-induced metabolic and vascular defects. Interestingly, wild-type female mice expressed markedly reduced levels of TRAF3IP2 mRNA independent of diet and were protected against high fat/high sucrose diet-induced vascular dysfunction. These data indicate that TRAF3IP2 plays a causal role in vascular insulin resistance and dysfunction. Specifically, the present findings highlight a sexual dimorphic role of TRAF3IP2 in vascular control and identify it as a promising therapeutic target in vasculometabolic derangements associated with obesity, particularly in males.

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Muscle‐specific sirtuin 3 overexpression does not attenuate the pathological effects of high‐fat/high‐sucrose feeding but does enhance cardiac SERCA2a activity

Physiological Reports ◽

10.14814/phy2.14961 ◽

2021 ◽

Vol 9 (16) ◽

Author(s):

Christopher J. Oldfield ◽

Teri L. Moffatt ◽

Kimberley A. O'Hara ◽

Bo Xiang ◽

Vernon W. Dolinsky ◽

...

Keyword(s):

High Fat ◽

Sirtuin 3 ◽

Sucrose Feeding ◽

High Sucrose Feeding ◽

High Sucrose

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SERUM LIPIDS DURING SHORT-TERM HIGH GLUCOSE AND HIGH SUCROSE FEEDING IN INFANTS

PEDIATRICS ◽

10.1542/peds.50.1.84 ◽

1972 ◽

Vol 50 (1) ◽

pp. 84-91

Author(s):

I. Tamir ◽

D. Epstein ◽

D. Heldenberg ◽

O. Levtow ◽

B. Werbin

Keyword(s):

High Glucose ◽

Caloric Intake ◽

Serum Triglyceride ◽

Normal Diet ◽

Total Serum ◽

Short Term ◽

Total Caloric Intake ◽

Sucrose Feeding ◽

High Sucrose Feeding ◽

High Sucrose

The effects of short-term high glucose and high sucrose diets on serum lipids were estimated in six healthy infants aged 4 to 11 months. Each carbohydrate-rich diet was given for 5 days and preceded by 3 days of a "normal" diet. During the high CHO feeding, sucrose or glucose supplied 73% of the total caloric intake, while on the "normal" diet only 40% for the total caloric intake was derived from CHO (glucose only). The percentage of total caloric intake supplied by protein was almost identical in the three diets used. An increase in serum triglyceride (TG) concentration, of almost equal magnitude, was seen following both high CHO feeding periods. Upon resumption of the "normal" diet, serum TG concentrations approached initial concentrations. No consistent changes occurred in total serum cholesterol concentrations or in total serum phospholipid concentrations. A significant increase in the percentage concentration of palmitoleic acid of serum triglyceride fatty acids occurred on both high CHO diets. This increase was slightly but not significantly greater following high sucrose feeding. A significant decrease in the percentage concentration of linoleic acid of serum triglyceride fatty acids occurred on both high CHO diets. This decrease was slightly but not significantly greater following high sucrose feeding. Therefore, it seems that on a short-term basis, high sucrose and high glucose feeding, in healthy infants, will result in similar changes in serum triglyceride concentrations and serum triglyceride fatty acid patterns.

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Maternal conjugated linoleic acid supplementation reverses high-fat diet-induced skeletal muscle atrophy and inflammation in adult male rat offspring

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00351.2015 ◽

2016 ◽

Vol 310 (5) ◽

pp. R432-R439 ◽

Cited By ~ 11

Author(s):

C. A. Pileggi ◽

S. A. Segovia ◽

J. F. Markworth ◽

C. Gray ◽

X. D. Zhang ◽

...

Keyword(s):

Skeletal Muscle ◽

Linoleic Acid ◽

Conjugated Linoleic Acid ◽

Muscle Development ◽

Maternal Diet ◽

Male Rat ◽

Skeletal Muscle Development ◽

High Fat ◽

Rat Offspring ◽

Total Fat

A high-saturated-fat diet (HFD) during pregnancy and lactation leads to metabolic disorders in offspring concomitant with increased adiposity and a proinflammatory phenotype in later life. During the fetal period, the impact of maternal diet on skeletal muscle development is poorly described, despite this tissue exerting a major influence on life-long metabolic health. This study investigated the effect of a maternal HFD on skeletal muscle anabolic, catabolic, and inflammatory signaling in adult rat offspring. Furthermore, the actions of maternal-supplemented conjugated linoleic acid (CLA) on these measures of muscle phenotype were investigated. A purified control diet (CD; 10% kcal fat), a CD supplemented with CLA (CLA; 10% kcal fat, 1% total fat as CLA), a high-fat (HFD; 45% kcal fat from lard), or a HFD supplemented with CLA (HFCLA; 45% kcal fat from lard, 1% total fat as CLA) was fed ad libitum to female Sprague-Dawley rats for 10 days before mating and throughout gestation and lactation. Male offspring received a standard chow diet from weaning, and the gastrocnemius was collected for analysis at day 150. Offspring from HF and HFCLA mothers displayed lower muscular protein content accompanied by elevated monocyte chemotactic protein-1, IL-6, and IL-1β concentrations. Phosphorylation of NF-κBp65 (Ser536) and expression of the catabolic E3 ligase muscle ring finger 1 (MuRF1) were increased in HF offspring, an effect reversed by maternal CLA supplementation. The present study demonstrates the importance of early life interventions to ameliorate the negative effects of poor maternal diet on offspring skeletal muscle development.

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