Hydrogen Sulfide in the Adipose Tissue-Physiology, Pathology and a Target for Pharmacotherapy

• Published in: Molecules (Basel, Switzerland) Switzerland), 2016-12, Vol.22 (1), p.63
• Main Authors: Bełtowski, Jerzy, Jamroz-Wiśniewska, Anna
• Format: Article
• Language: English
• Subjects: Adenosine; Adipocytes; Adipocytes - cytology; adipogenesis; Adipogenesis - physiology; Adipose tissue; Adipose Tissue - metabolism; Cyclic AMP; Cytokines; Drug therapy; Energy; Enzymes; Fatty acids; Glucose; Glucose - metabolism; Glycerol; Hormones; Humans; Hydrogen; Hydrogen sulfide; Hydrogen Sulfide - metabolism; Hyperglycemia; Hyperglycemia - pathology; Insulin; Insulin resistance; Insulin Resistance - physiology; Kinases; Lipids; lipolysis; Lipolysis - physiology; Metabolic disorders; Metabolic syndrome; Metabolic Syndrome - pathology; Mitochondria; Muscle, Smooth - metabolism; Muscles; Nervous system; Nitric oxide; Obesity; Obesity - pathology; Peptides; Physiology; Potassium Channels, Voltage-Gated - metabolism; Proteins; Review; Triglycerides; Tumor necrosis factor-TNF; vascular tone
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules22010063

Hydrogen sulfide (H₂S) is synthesized in the adipose tissue mainly by cystathionine γ-lyase (CSE). Several studies have demonstrated that H₂S is involved in adipogenesis, that is the differentiation of preadipocytes to adipocytes, most likely by inhibiting phosphodiesterases and increasing cyclic AMP concentration. The effect of H₂S on adipose tissue insulin sensitivity and glucose uptake is controversial. Some studies suggest that H₂S inhibits insulin-induced glucose uptake and that excess of H₂S contributes to adipose tissue insulin resistance in metabolic syndrome. In contrast, other studies have demonstrated that H₂S stimulates glucose uptake and its deficiency contributes to insulin resistance. Similarly, the effect of H₂S on adipose tissue lipolysis is controversial. H₂S produced by perivascular adipose tissue decreases vascular tone by activating ATP-sensitive and/or voltage-gated potassium channels in smooth muscle cells. Experimental obesity induced by high calorie diet has a time dependent effect on H₂S in perivascular adipose tissue; short and long-term obesity increase and decrease H₂S production, respectively. Hyperglycemia has been consistently demonstrated to suppress CSE-H₂S pathway in various adipose tissue depots. Finally, H₂S deficiency may contribute to adipose tissue inflammation associated with obesity/metabolic syndrome.