Cissuslean®

Research

Pre-Clinical Research

Pre-clinical research established the mechanistic basis for Cissuslean® and its potential role in weight and metabolic health. Using adipocyte cell cultures and a high-fat-diet mouse model, researchers investigated effects on lipid accumulation, adipogenic signaling, body fat, biochemical markers and adipose tissue.

Inhibition of lipid accumulation in adipocytes

Model
Differentiated 3T3-L1 and NIH/3T3 adipocyte models
Objective
Determine whether Cissuslean® could reduce triglyceride accumulation during adipocyte differentiation and influence cellular fat storage.
Findings
Cissuslean® reduced intracellular triglyceride accumulation in a concentration-dependent manner. Cell-viability testing found no significant loss of metabolic activity or visible cytotoxic changes across the concentrations evaluated.
Relevance
Suggests Cissuslean® can influence fat-storage processes directly at the cellular level.

Modulation of adipogenesis and lipid-metabolism pathways

Model
3T3-L1 adipocytes; Western blot analysis
Objective
Investigate how Cissuslean® affects proteins involved in adipogenesis, lipogenesis, fatty-acid oxidation and metabolic inflammation.
Findings
Cissuslean® increased PPARα expression and AMPK phosphorylation while reducing PPARγ expression and AKT phosphorylation. It also increased ACC phosphorylation (reduced fatty-acid synthesis) and lowered NF-κB phosphorylation. Most effects were concentration-dependent.
Relevance
Coordinated mechanism involving reduced adipocyte formation and lipid synthesis, together with increased fatty-acid oxidation.

Effects in high-fat-diet-induced obese mice

Model
Male C57BL/6J mice, 25/50/100 mg/kg oral doses
Objective
Evaluate body composition, liver-related biochemical markers, blood glucose and lipid parameters in a high-fat-diet-induced obesity model.
Findings
Cissuslean® therapy reduced high-fat-diet-associated elevations in ALT and AST relative to the untreated high-fat-diet group. Dose-dependent mitigation of obesity-related liver and metabolic abnormalities was reported at 50 and 100 mg/kg.
Relevance
Provides in vivo support for the metabolic effects observed in adipocyte models.

Move from mechanism to human evidence