Energy balance
Genetic deficiency of the enzyme CD38 protects against high-fat diet-induced obesity by enhancing energy expenditure and preventing glucose intolerance.
This research suggests that the enzyme CD38 plays a critical role in how our bodies store fat when eating a high-fat diet. By depleting NAD, CD38 inhibits the SIRT1-PGC1alpha pathway, which is responsible for burning energy and creating mitochondria. Inhibiting CD38 (as seen in knockout mice) prevents obesity even on a high-fat diet. For humans, this highlights the importance of NAD levels and SIRT1 activity (potentially influenced by exercise or compounds like resveratrol) in managing weight, rather than just caloric intake alone.
We report that CD38-deficient mice are protected against high-fat diet-induced obesity owing to enhanced energy expenditure.
Why this rating
High-quality animal model data with rigorous calorimetric and biochemical assays, though not human clinical data.
Source
The enzyme CD38 (a NAD glycohydrolase, EC 3.2.2.5) is necessary for the development of diet‐induced obesity
Maria Thereza Barbosa et al. · The FASEB Journal · 2007
DOI 10.1096/fj.07-8290com
More from this paper
Related findings · Energy balance
- Achieving a total body weight loss of 10-15% (or >10-15 kg) through Total Diet Replacement (TDR) induces remission of Type 2 Diabetes in individuals with short-duration disease.Strong
- Bariatric surgery is superior to medical management alone for inducing significant long-term weight loss, remission of type 2 diabetes, and reduction in mortality for patients with BMI ≥ 40 or ≥ 35 with comorbidities.Strong
- Achieving type 2 diabetes remission requires significant weight loss (≥15 kg) via major caloric restriction, independent of macronutrient composition.Strong
This is one finding among thousands. Every one is graded and traced to its source, so you can see what the evidence actually supports. Browse the research →