This study provides evidence that dairy limits weight gain to a similar extent as exercise training and the combined effects are greater than either intervention alone. While exercise training reduces weight gain through increases in energy expenditure, dairy appears to increase lipid excretion in the feces.
Objective This study aimed to explore the individual and combined effects of skim milk powder (SMP) and exercise on indices of systemic and liver lipid metabolism in male obese rats. Methods Rats were fed a high‐fat (~ 40% kcal from fat), high‐sugar diet for 8 weeks. At 12 weeks of age, rats were assigned to one of four weight‐matched, isocaloric, high‐fat, high‐sugar groups for 6 weeks: (1) casein‐sedentary, (2) casein‐exercise, (3) SMP‐sedentary, and (4) SMP‐exercise. Nonfat SMP or casein was the sole protein source in the dairy and control casein diets, respectively. Exercise training occurred 5 d/wk for 60 minutes on a motorized treadmill. Whole‐body metabolism was assessed by a Comprehensive Lab Animal Monitoring System. Lipidomics, Western blot, and polymerase chain reaction were used to assess markers of hepatic lipid metabolism. Results Exercise, but not SMP, altered the fatty acid composition of liver triglycerides, reduced indices of lipogenesis, and increased expression of genes linked to oxidative metabolism, in conjunction with increases in whole‐body fat oxidation. SMP and exercise reduced plasma triglycerides in an additive manner. Conclusions These findings provide evidence that SMP and exercise exert distinct effects on whole‐body and hepatic carbohydrate and lipid metabolism and that they could work in a synergistic manner to reduce serum triglyceride concentrations.
Energy imbalance is a primary cause of obesity. While the classical approach to attenuate weight gain includes an increase in energy expenditure through exercise, dietary manipulation such as the inclusion of dairy products has also been proven effective. In the present study, we explored the potential mechanisms by which dairy and exercise attenuate weight gain in diet-induced obese rats. Male Sprague-Dawley rats were fed a high fat, high-sugar (HFHS) diet to induce obesity for 8 weeks. Rats were then further grouped into either control (HFHS + casein) or dairy diet (HFHS + nonfat skim milk) with and without treadmill exercise for 6 weeks. Serum and fresh fecal samples were collected for gut microbiota, serum metabolomics, and metallomics analysis. Diet and exercise resulted in distinct separation in both gut microbiota and serum metabolite profiles. Most intriguingly, obesogenic bacteria including Desulfovibrio and Oribacterium were reduced, and bioactive molecules such as mannose and arginine were significantly increased in the dairy group. Correlations of at least six bacterial genera with serum metal ions and metabolites were also found. Results reveal distinct impacts of dairy and exercise on the gut microbiota and in the modulation of circulating metabolites with the former primarily responsible for driving microbial alterations known to attenuate weight gain.
These findings suggest that previous training increases adipose tissue beta-adrenergic responsiveness to a short-term HFD. This may help to explain the protective effect of prior exercise training against the deleterious effects of a HFD.
Even if we can affect the human microbiome in positive ways through exercise, the microbiome tends to to remain relatively stable within a few years after birth, and seems to only temporarily respond to select stimuli (like exercise, diet, and antibiotics). Promisingly, metabolic benefits were observed when gut bacteria were transplanted from lean donors into recipients with metabolic syndrome (2). But while the transplantation of microbiomes may work in humans, this procedure remains controversial... and icky. These results raise the intriguing question of whether it is possible to engineer an 'ideal' microbiome that would be capable of harvesting sufficient energy and nutrients from the diet, but make one resistant to obesity and T2D. For example, we could reduce the quantity of Erysipelotrichaceae and Turicibacteraceae, two bacterial families associated with obesity and gut inflammation. Or it may be as simple as engineering greater microbial diversity, as this is decreased in obese and diabetic individuals. Despite probiotics and prebiotics being commercially available for decades, research into the relationship between host and microbiome is relatively young, but there are already extremely promising results. Who knows, one day we may all be popping pills full of gut germs to try and stay healthy!
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