La suplementación con zinc reduce la concentración de ácidos grasos libres en pacientes con diabetes tipo 2

RESUMEN Elevadas concentraciones de ácidos grasos libres (AGL) han sido asociadas con la patogénesis de resistencia a la insulina y diabetes tipo 2 (DT2), por lo que la regulación de la lipólisis resulta prioritaria en estos pacientes. El zinc mediante sus acciones insulinomiméticas e inducción de fosfodiesterasas podría regular la liberación de AGL desde el tejido adiposo. El objetivo de esta investigación fue evaluar en pacientes con DT2 el efecto de 24 meses de suplementación con zinc sobre las concentraciones séricas de AGL en ayuno. Para este propósito: se realizó la determinación de AGL en ayuno por colorimetría enzimática, zinc plasmático por espectrofotometría de absorción atómica, y parámetros bioquímicos y antropométricos de interés en 60 pacientes con DT2 que fueron asignados aleatoriamente para recibir suplementación con 30 mg/día de zinc (n= 30) o placebo (n= 30) por 24 meses. El grupo zinc presentó menor concentración sérica de AGL al mes 24 (p = 0,034). El cambio en el índice de masa corporal, el sexo y la suplementación con zinc contribuyeron significativamente como predictores de la concentración sérica de AGL al mes 24 (R= 0,493, R2= 0,243, p= 0,001). Conclusión: la suplementación con 30 mg/día de zinc en pacientes con DT2 tuvo un efecto significativo en reducir la concentración sérica de AGL en ayuno tras 24 meses de tratamiento. Estos resultados apoyan los beneficios del zinc como coadyuvante en el tratamiento de DT2.

ABSTRACT High concentrations of free fatty acids (FFA) have been associated with the pathogenesis of insulin resistance and type 2 diabetes (T2D), making lipolysis regulation a priority in these patients. Through its insulin-mimetic actions and phosphodiesterase induction, zinc could regulate FFA release from adipose tissue. The objective of this research was to evaluate the effect of 24 months of zinc supplementation on fasting serum FFA concentrations in patients with T2D. For this purpose: fasting FFA by enzymatic colorimetric, plasma zinc by atomic absorption spectrophotometry, and biochemical and anthropometric parameter of interest were determined in 60 T2D patients who were randomly assigned to 30 mg/day of zinc supplementation (n= 30) or placebo (n= 30) for 24 months. The zinc group had lower serum FFA concentration at month 24 (p= 0.034). Body mass index change, gender, and zinc supplementation contributed significantly as predictors of serum FFA concentration at month 24 (R= 0.493, R2= 0.243, p= 0.001). Conclusion: Supplementation with 30 mg/day of zinc in patients with T2D had a significant effect in reducing serum fasting FFA concentration after 24 months of treatment. These results support the benefits of zinc as coadjutant in T2D treatment.

Fatty acid desaturation in red blood cell membranes of patients with type 2 diabetes is improved by zinc supplementation.

BACKGROUND/OBJECTIVE: Membrane flexibility can be a determining factor in pathophysiological mechanisms of type 2 diabetes (T2D). As a cofactor of delta-5 desaturase (D5D) and delta-6 desaturase (D6D), and gene expression regulator, zinc may play a role modulating membrane flexibility by increasing membrane polyunsaturated fatty acids (PUFA) abundance. The objective of this study was to evaluate the effect of a 24-month zinc supplementation (30 mg elemental zinc) on membrane fatty acid composition in patients with T2D. SUBJECTS/METHODS: Sixty patients with T2D were evaluated. Thirty were randomly assigned to the zinc supplemented group and thirty to the placebo group. Fatty acid composition in red blood cell (RBC) membranes was determined by gas chromatography. Expression of gene encoding for D5D (FADS1), and D6D (FADS2) were evaluated in peripheral blood mononuclear cells by real-time polymerase chain reaction. RESULTS: After 24 months of supplementation, a greater abundance of docosapentaenoic acid (C22:5 n-3), arachidonic acid (C20:4 n-6), adrenic acid (C22:4 n-6), and total n-6 PUFA was found (p = 0.001, p = 0.007, p = 0.033, p = 0.048, respectively). The unsaturated fatty acids/saturated fatty acids ratio, and unsaturation index was increased in the zinc supplemented group at month 24 (p = 0.003 and p  = 0.000, respectively). FADS1 gene was upregulated in the zinc group in relation to placebo at month 12 (p = 0.020). CONCLUSIONS: Supplementation with 30 mg/d elemental zinc during 24 months in patients with T2D had an effect on the composition of RBC membranes increasing PUFA abundance and in turn, improving membrane flexibility. This effect may be mediated by induction of D5D gene expression.

Nutritional Effects of Zinc on Metabolic Syndrome and Type 2 Diabetes: Mechanisms and Main Findings in Human Studies.

Zinc (Zn) plays crucial roles in mammalian metabolism. There is increasing interest about the potential beneficial effects of Zn on the prevention or treatment of non-communicable diseases. This review critically analyzes the information related to the role of Zn on the metabolic syndrome (MetS) as well as type 2 diabetes (T2D), and summarizes the biological basis of these potential effects of Zn. There are several mechanisms by which Zn may help to prevent the development or progression of MetS and T2D, respectively. Zn is involved in both insulin secretion and action in peripheral tissues. Specifically, Zn has insulin-mimetic properties that increase the activity of the insulin signaling pathway. Zn modulates long-chain polyunsaturated fatty acids levels through its action on the absorption of essential fatty acids in the intestine and its subsequent desaturation. Zn is also involved in both the assembly of chylomicrons and lipoproteins as well as their clearance, and thus, plays a role in lipolysis regulation. Finally, Zn has been found to play a role in redox metabolism, and in turn, on blood pressure. The evidence related to the association between Zn status and occurrence of MetS is inconsistent. Although there are several studies reporting an inverse relationship between Zn status or dietary Zn intake and MetS prevalence, others found a direct relationship between Zn status and MetS prevalence. Intervention studies also provide confusing information about this issue, making it hard to reach firm conclusions. Zn as part of the treatment for patients with T2D has been shown to have positive responses in terms of glucose control outcomes, but only among those with Zn deficiency.