Obesity is characterised by metabolic dysfunction that includes insulin and leptin resistance. This dysfunction leads to a derailing of normal appetite and energy regulation and this results in hyperphagia and reductions in resting, postprandial and post-exercise metabolic rates. This is the central driver of weight gain and any effort to lose body fat will be severely hampered until this dysfunction is corrected. The Western diet is thought to be the cause of the metabolic dysfunction seen in obesity, characterised as it is my low quality processed foods containing metabolic poisons. These foods are also deficient in micronutrients and this exacerbates the underlying metabolic dysfunction. This is because vitamins and minerals are required as cofactors in metabolic pathways and in this role they allow these pathways to flow. Deficiency of any micronutrient required as a cofactor in a metabolic pathways can limit the flux through that pathways and this is a contributory factor in the metabolic dysfunction seen in obesity.
A number of nutrients are associated with obesity, which can be thought of as nutrient deficient state. Epidemiological studies suggest that zinc levels of obese subjects are low compared to normal weight individuals. This may result from nutrient poor foods providing a low zinc intake in combination with the chronic inflammation associated with obesity which can deplete zinc stores and shift zinc balance towards negative. Research has investigated the effects of a chronic zinc deficiency on parameters of obesity in overweight mice1. Mice were fed a high fat obesogenic diet that caused weight gain, and then a treatment group was exposed to a zinc deficient diet while a control group received adequate zinc nutrition. The results showed that zinc deficiency caused changes to the metabolism of the mice which may have had detrimental effects on their condition. In particular, the zinc deficient mice showed an increase in circulating leptin and increased leptin signalling in their livers.
Leptin is a hormone that acts as a feedback signal to inform the brain of body fat levels. As body fat increases more leptin is released and this causes counter regulatory mechanisms to lower fat reserves. These mechanisms include increased physical activity, increased metabolic rate and decreased appetite. However, obesity is characterised by leptin resistance, whereby the signal from the leptin hormone becomes weaker and as a result leptin levels rise to higher than normal values. Obese individuals therefore paradoxically have higher levels of leptin compared to lean counterparts. From these results it appears that zinc is involved in leptin signalling in some way in mice, and this results in increased leptin levels and increased leptin signalling in the liver. Another finding of this study was the increased macrophage infiltration to fat tissue caused by zinc deficiency. This infiltration is a cause of the inflammation seen in obesity. Zinc deficiency may therefore exacerbate some of the metabolic changes seen in obesity.
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