Effects of Berberine on Insulin-Sensitive Tissues: Nutrient-Derived Modulator of Metabolic Disease
- 1Department of Health Sciences, Faculty of Applied Health Sciences, Brock University, St. Catharines, ON L2S 3A1, Canada
- 2Centre for Bone and Muscle Health, Applied Health Sciences, Brock University, St. Catharines, ON L2S 3A1, Canada
Abstract
Insulin-sensitive tissues, including skeletal muscle, adipose tissue, and liver, are central regulators of systemic glucose and lipid homeostasis. Insulin signaling disruption in these tissues is a key pathological feature underlying insulin resistance and contributes to the development of metabolic disorders such as type 2 diabetes mellitus (T2DM), obesity, and liver disease. Increasing evidence suggests that berberine (BBR), a naturally occurring isoquinoline alkaloid derived from Berberis species, attenuates insulin resistance and exhibits antidiabetic, lipid-lowering, and anti-inflammatory properties across multiple metabolic tissues. This review analyzes current in vitro, in vivo, and clinical data examining the effects of BBR in insulin-sensitive tissues. In skeletal muscle, BBR promotes glucose consumption while in adipose tissue, it attenuates adipogenesis, lipid accumulation and inflammation. In hepatic tissue, BBR suppresses gluconeogenesis, improves lipid metabolism and reduces hepatic steatosis. Clinical trials report reductions in fasting glucose, serum lipids, visceral adiposity, and hepatic fat content. Collectively, current evidence indicates that BBR exerts multi-tissue insulin-sensitizing effects with therapeutic potential for metabolic disease. However, mechanistic human data directly linking tissue-specific actions remain limited. Future clinical studies incorporating tissue-specific metabolic assessments, dose–response analyses, metabolomic profiling, and consideration of sex- and age-related variability are warranted to fully elucidate its clinical efficacy.
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BibTeX
@article{harrison2026effects,
title = {{Effects of Berberine on Insulin-Sensitive Tissues: Nutrient-Derived Modulator of Metabolic Disease}},
author = {Maddox Harrison and Nicolaos Achilleos and Evangelia Tsiani},
journal = {Cells},
year = {2026},
month = oct,
doi = {10.3390/cells15211984},
url = {https://www.mdpi.com/2073-4409/15/21/1984},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Effects of Berberine on Insulin-Sensitive Tissues: Nutrient-Derived Modulator of Metabolic Disease
AU - Maddox Harrison
AU - Nicolaos Achilleos
AU - Evangelia Tsiani
PY - 2026
DA - 2026/10/30
JO - Cells
DO - 10.3390/cells15211984
UR - https://www.mdpi.com/2073-4409/15/21/1984
AB - Insulin-sensitive tissues, including skeletal muscle, adipose tissue, and liver, are central regulators of systemic glucose and lipid homeostasis. Insulin signaling disruption in these tissues is a key pathological feature underlying insulin resistance and contributes to the development of metabolic disorders such as type 2 diabetes mellitus (T2DM), obesity, and liver disease. Increasing evidence suggests that berberine (BBR), a naturally occurring isoquinoline alkaloid derived from Berberis species, attenuates insulin resistance and exhibits antidiabetic, lipid-lowering, and anti-inflammatory properties across multiple metabolic tissues. This review analyzes current in vitro, in vivo, and clinical data examining the effects of BBR in insulin-sensitive tissues. In skeletal muscle, BBR promotes glucose consumption while in adipose tissue, it attenuates adipogenesis, lipid accumulation and inflammation. In hepatic tissue, BBR suppresses gluconeogenesis, improves lipid metabolism and reduces hepatic steatosis. Clinical trials report reductions in fasting glucose, serum lipids, visceral adiposity, and hepatic fat content. Collectively, current evidence indicates that BBR exerts multi-tissue insulin-sensitizing effects with therapeutic potential for metabolic disease. However, mechanistic human data directly linking tissue-specific actions remain limited. Future clinical studies incorporating tissue-specific metabolic assessments, dose–response analyses, metabolomic profiling, and consideration of sex- and age-related variability are warranted to fully elucidate its clinical efficacy.
SN - 2073-4409
ER -