Description: |
Stearic Acid and its derivatives have been used as gelators in food and pharmaceutical gel formulations. Stearic Acid is a potent phosphatase 1B inhibitor, possibly causing an enhancement in the insulin receptor signaling to stimulate glucose uptake into adipocytes. Stearic Acid leads to dramatically reduced visceral fat likely by causing the apoptosis of preadipocytes, it also can reduce metastatic tumor burden.
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Targets: |
Caspase | GLUT | Akt | MCP-1 |
In vitro: |
Cell Physiol Biochem. 2013;32(5):1451-9. | Stearic acid serves as a potent inhibitor of protein tyrosine phosphatase 1B.[Pubmed: 24296476] | Free fatty acids (FFAs) are implicated in diverse signal transduction pathways. The present study investigated the effects of the saturated FFA Stearic Acid on protein tyrosine phosphatase 1B (PTP1B) activity, Akt activity, and glucose uptake into cells relevant to insulin signal. METHODS AND RESULTS: PTP1B activity was assayed under the cell-free conditions. Phosphorylation of insulin receptor and Akt and glucose uptake into cells were monitored in differentiated 3T3-L1-GLUT4myc adipocytes. In the cell-free PTP1B assay, Stearic Acid suppressed PTP1B activity in a concentration (1-30 μM)-dependent manner. For 3T3-L1- GLUT4myc adipocytes insulin phosphorylated insulin receptor at Tyr1185 and Akt at Thr308 and Ser473 in a concentration (100 fM-100 nM)-dependent manner and stimulated glucose uptake into cells in a concentration (0.1-100 nM)-dependent manner. Stearic Acid (30 μM) significantly increased insulin-induced phosphorylation of insulin receptor at Tyr1185, but insulin-induced phosphorylation of Akt was not significantly enhanced. Stearic Acid (30 μM) by itself promoted glucose uptake into adipocytes. CONCLUSIONS: The results of the present study indicate that Stearic Acid serves as a potent PTP1B inhibitor, possibly causing an enhancement in the insulin receptor signaling to stimulate glucose uptake into adipocytes. |
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In vivo: |
PLoS One. 2014 Sep 15;9(9):e104083. | Dietary stearic acid leads to a reduction of visceral adipose tissue in athymic nude mice.[Pubmed: 25222131] | Stearic acid (C18:0) is a long chain dietary saturated fatty acid that has been shown to reduce metastatic tumor burden. METHODS AND RESULTS: Based on preliminary observations and the growing evidence that visceral fat is related to metastasis and decreased survival, we hypothesized that dietary stearic acid may reduce visceral fat. Athymic nude mice, which are used in models of human breast cancer metastasis, were fed a stearic acid, linoleic acid (safflower oil), or oleic acid (corn oil) enriched diet or a low fat diet ad libitum. Total body weight did not differ significantly between dietary groups over the course of the experiment. However visceral fat was reduced by ~70% in the stearic acid fed group compared to other diets. In contrast total body fat was only slightly reduced in the stearic acid diet fed mice when measured by dual-energy x-ray absorptiometry and quantitative magnetic resonance. Lean body mass was increased in the stearic acid fed group compared to all other groups by dual-energy x-ray absorptiometry. Dietary stearic acid significantly reduced serum glucose compared to all other diets and increased monocyte chemotactic protein-1 (MCP-1) compared to the low fat control. The low fat control diet had increased serum leptin compared to all other diets. To investigate possible mechanisms whereby stearic acid reduced visceral fat we used 3T3L1 fibroblasts/preadipocytes. Stearic acid had no direct effects on the process of differentiation or on the viability of mature adipocytes. However, unlike oleic acid and linoleic acid, stearic acid caused increased apoptosis (programmed cell death) and cytotoxicity in preadipocytes. The apoptosis was, at least in part, due to increased caspase-3 activity and was associated with decreased cellular inhibitor of apoptosis protein-2 (cIAP2) and increased Bax gene expression. CONCLUSIONS: In conclusion, dietary stearic acid leads to dramatically reduced visceral fat likely by causing the apoptosis of preadipocytes. |
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