Abstract
Spilanthol (SP) is a bioactive compound found in Spilanthes acmella, giving the flowers and leaves a spicy taste. Studies found that phyto-ingredients stored in spice plants act against obesity-related diseases. SP has antimicrobial, anti-inflammatory, and analgesic properties, but the effects on obesity are not yet known. We investigated the effects of SP in differentiated adipocytes (3T3-L1 cells) and mice fed a high-fat diet (HFD). SP significantly inhibited intracellular lipid accumulation and significantly reduced the expression of lipogenesis-related proteins, including acetyl-CoA carboxylase (ACC) and fatty-acid synthase (FAS). In contrast, SP increased the expression of carnitine palmitoyltransferase (CPT)1 and AMP-activated protein kinase (AMPK) in adipocytes. However, SP suppressed the levels of cyclooxygenase-2 (COX-2), phospho-p38 (pp38), and phospho-JNK (c-Jun N-terminal kinase) (pJNK) in LPS (lipopolysaccharide)-stimulated murine pre-adipocytes. SP administered to HFD-induced obese mice via intraperitoneal injections twice a week for 10 weeks decreased body weight gain, visceral adipose tissue weight, and adipocyte size. SP inhibited lipogenic proteins FAS and ACC, and suppressed adipogenic transcription factors, enhancing lipolysis and AMPK protein expression in the liver. SP has anti-obesity effects, upregulating AMPK to attenuate lipogenic and adipogenic transcription factors.
Highlights
Obesity is caused by excessive triglyceride (TG) accumulation, primarily due to imbalanced energy homeostasis
We investigated whether spilanthol modulates lipogenesis and adipogenesis in differentiated adipocytes and improves the metabolic profile of visceral adipose tissue in high-fat diet (HFD)-induced obese mice (Figure 1A)
We evaluated whether spilanthol enhances AMPK and carnitine palmitoyltransferase 1 (CPT1) expression in 3T3-L1 cells and found that the protein expression of both was significantly increased in the presence of spilanthol compared to control differentiated adipocytes (Figure 3B,C)
Summary
Obesity is caused by excessive triglyceride (TG) accumulation, primarily due to imbalanced energy homeostasis. Obesity is one of the most prevalent diseases worldwide [1] and causes chronic inflammatory reactions, which activate T-cell and macrophage infiltration into adipose tissues, resulting in the release of inflammatory mediators, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and monocyte chemoattractant protein (MCP)-1, from adipose tissue [2]. Insulin resistance is induced by obesity–leptin resistance, which activates the inflammatory mitogen-activated protein. Obesity-induced cytokines, especially MCP-1, promote anti-inflammatory M2 macrophage transformation into inflammatory M1 macrophages with increasing obesity-induced inflammation and the expression of a variety of proteins, such as cyclooxygenase-2. Obesity-induced inflammation is associated with the development of insulin resistance, type 2 diabetes, hypertension, atherothrombosis, and chronic inflammatory diseases [5,6]. Obesity is a complex multifactorial disease, but novel therapeutic dietary interventions may have anti-inflammatory components that are beneficial
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