RESUMO
Introduction: Initially known for its deleterious health effects, hydrogen sulfide (H2S) has recently been recognized as a biologically important gas carrier, like nitric oxide and carbon monoxide. H2S is produced endogenously in mammalian cells by enzymatic and non-enzymatic pathways. When it is produced by the enzymatic pathway, its synthesis is carried out from the amino acid L-cysteine through the transsulfuration pathway. It can also be produced endogenously from exogenous compounds that function as H2S donors as, for example, the naturally occurring organic donors found in some plants. Currently, the role of S2H is well known as brain and cardiac protector, and its research as a therapeutic adjuvant in metabolic diseases such as obesity and type-2 diabetes is becoming increasingly important. The objective of this review is to examine how the contribution of donors and precursors of hydrogen sulfide by the diet impacts health and disease.
Introducción: Conocido originalmente por sus efectos deletéreos en la salud, recientemente se ha reconocido al sulfuro de hidrógeno (H2S) como un gasotransmisor de importancia biológica, al igual que el óxido nítrico y el monóxido de carbono. El H2S puede producirse de forma endógena en las células de mamíferos por dos vías: la vía enzimática y la vía no enzimática. Cuando se produce por la vía enzimática, su síntesis se lleva a cabo a partir de los aminoácidos L-cisteína o metionina mediante transulfuración y transmetilación. También se puede producir el H2S a partir donadores de grupos sulfuro como, por ejemplo, compuestos orgánicos que se encuentran presentes en algunos vegetales. Actualmente es bien conocido el papel del H2S como protector a nivel cerebral y cardiaco, y cada vez adquiere mayor relevancia su estudio como coadyuvante terapéutico en padecimientos metabólicos como la obesidad y la diabetes mellitus de tipo 2. El objetivo de esta revisión es examinar cómo impacta el aporte de donadores y precursores del sulfuro de hidrogeno por la dieta en la salud y la enfermedad.
RESUMO
Metabolic syndrome (MS) is a condition that includes obesity, insulin resistance, dyslipidemias among other, abnormalities that favors type 2 Diabetes Mellitus (T2DM) and cardiovascular diseases development. Three main diet-induced metabolic syndrome models in rats exist: High carbohydrate diet (HCHD), high fat diet (HFD), and high carbohydrate-high fat diet (HCHHFD). We analyzed data from at least 35 articles per diet, from different research groups, to determine their effect on the development of the MS, aimed to aid researchers in choosing the model that better suits their research question; and also the best parameter that defines obesity, as there is no consensus to determine this condition in rats. For the HCHD we found a mild effect on body weight gain and fasting blood glucose levels (FBG), but significant increases in triglycerides, fasting insulin, insulin resistance and visceral fat accumulation. HFD had the greater increase in the parameters previously mentioned, followed by HCHHFD, which had a modest effect on FBG levels. Therefore, to study early stages of MS a HCHD is recommended, while HFD and HCHHFD better reproduce more severe stages of MS. We recommend the assessment of visceral fat accumulation as a good estimate for obesity in the rat.