Energy balance
Pharmacological inhibition or genetic deficiency of Stearoyl-CoA desaturase 1 (SCD1) reduces body adiposity and prevents diet-induced obesity by increasing energy expenditure and fatty acid oxidation.
Current research suggests that targeting the SCD1 enzyme could be a viable strategy for treating obesity. In animal models, reducing SCD1 activity leads to increased fat burning and resistance to weight gain, even with high food intake. While not yet a human treatment, this highlights the importance of lipid metabolism enzymes in body weight regulation.
SCD1-deficient mice have increased energy expenditure, reduced body adiposity, increased insulin sensitivity and are resistant to diet-induced obesity and liver steatosis.
Why this rating
Evidence is derived from murine models (SCD1-/- mice and ob/ob mice); human clinical data is not provided.
Source
Stearoyl‐CoA desaturase as a new drug target for obesity treatment
Agnieszka Dobrzyń et al. · Obesity Reviews · 2005
DOI 10.1111/j.1467-789x.2005.00177.x
More from this paper
- Inhibition of Stearoyl-CoA desaturase 1 (SCD1) protects against hepatic steatosis (fatty liver) by decreasing de novo fatty acid synthesis and increasing fatty acid oxidation.Moderate
- Deficiency in Stearoyl-CoA desaturase 1 (SCD1) improves insulin sensitivity and glucose tolerance in skeletal muscle.Moderate
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