Department of Clinical Chemistry and Hematology, Pharos University in Alexandria, Al Shri Al Omomi, Qism Sidi Gabir, Alexandria Governorate, EgyptEgypt
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Obesity has been identified as a medical problem. Obesity may be associated with abnormal metabolism and micronutrient deficiencies. Thus, obesity and malnutrition at the same time is a reality. However, in the past it was unusual to say that people who eat much were liable to be malnourished. Now-a-days, eating too much does not mean meeting nutritional requirements. This is due to the fact that several factors affect those requirements; as nature of diet, dietary habits, food preparation and host-related factors as intestinal absorption.
Keywords: hormones; enzymes
Letter to the Editor Obesity and Trace Elements * *Corresponding author Hala Mourad Demerdash, PhD * Hala Mourad Demerdash Associate Professor Department of Clinical Chemistry and Hematology Department of Clinical Chemistry and Hematology, Pharos University in Alexandria, Al Shri Al Pharos University in Alexandria Omomi, Qism Sidi Gabir, Alexandria Governorate, Egypt Al Shri Al Omomi, Qism Sidi Gabir Alexandria Governorate, Egypt E-mail: demerdashh@yahoo.com Obesity has been identified as a medical problem. Obesity may be associated with ab- Volume 2 : Issue 3 normal metabolism and micronutrient deficiencies. Thus, obesity and malnutrition at the same Article Ref. #: 1000OROJ2115 time is a reality. However, in the past it was unusual to say that people who eat much were liable to be malnourished. Now-a-days, eating too much does not mean meeting nutritional require- ments. This is due to the fact that several factors affect those requirements; as nature of diet, Article History th dietary habits, food preparation and host-related factors as intestinal absorption. Received: October 26 , 2015 th Accepted: October 28th, 2015 th Trace elements are of great value in regulation of normal body metabolism, as they Published: October 28 , 2015 interact with many enzymes and hormones; some of which will be discussed. Citation MAGNESIUM Demerdash HM. Obesity and trace elements. Obes Res It is the second most abundant intracellular cation, approximately 50% of total body Open J. 2015; 2(3): 98-100.
doi: 10.17140/OROJ-2-115 magnesium is found in bones. The other 50% is found inside cells of body tissues and only 1% is found in blood. Magnesium is essential for absorption and utilization of nutrients; car- bohydrates, fats and proteins. It is a critical cofactor for hundreds of enzymes especially those involved in glucose metabolism and a direct antagonist of intracellular calcium. Moreover, it is associated with insulin sensitivity. As hypomagnesaemia results in reduced insulin sensitivity of peripheral tissue through reduced auto-phosphorylation of tyrosine kinase, a component of the β-subunit of the insulin receptor for which magnesium is a co-factor. Also, hypomagnesae- mia may be associated with reduced β-cells proliferation and thus affecting insulin production. Therefore, serum magnesium levels are negatively correlated with Insulin Resistance (HOMA- IR).
The exact mechanism of hypomagnesaemia in obese patients is unclear but may be related to eating habits; as increased intake of carbonated soft drinks, which are rich in phos- phorous and thereby interfere with magnesium absorption, or increased intake of caffeine re- sulting in increased magnesium excretion. Another mechanism may be increased intake of dairy products with high Ca+ content and or fat content thus interfere with its absorption.1 IRON Iron is essential co-factor; it is a constituent of a number of important macromol- ecules, including those involved in energy production, Deoxyribonucleic acid (DNA) synthesis and metabolism. On the other hand, iron can be dangerous being a catalyst of free radical re- actions. Because of this dual nature, iron balance is tightly regulated. Most of iron in body is incorporated to heme biosynthesis in erythropoietic bone marrow and other heme containing Copyright enzymes, the remaining amount is found in hepatocytes and cells of reticuloendothelial system. ©2015 Demerdash HM. This is an open access article distributed un- der the Creative Commons Attribu- Obesity may promote iron deficiency through inhibition of dietary iron absorption tion 4.0 International License (CC from the duodenum. Under normal conditions, iron absorption is dependent on both a divalent BY 4.0), which permits unrestricted metal transporter and the iron exporter Ferroportin (FPN). FPN is regulated by hepcidin. The use, distribution, and reproduction in any medium, provided the origi- liver derived peptide hormone hepcidin is the primary regulator of iron hemostasis; which nal work is properly cited. is both an inhibitor of intestinal iron absorption as well as macrophage iron release. In the intestines hepcidin exerts its effect by binding to iron exporter and low serum zinc were associated with increased cardiovascu- ferroportin (FPN) leading to FPN phosphorylation, degradation lar mortality.5 and decreased iron absorption. Also pro-inflammatory cytokines secreted from adipose tissue in obese subjects stimulate hepci- Copper imbalance often results in a reduced desire for din release from adipose tissue. In addition, these cytokines as protein, especially animal protein. Also high tissue copper ag- Interleukin 1 (IL-1) and Interleukin 6 (IL-6) may interfere with gravates obesity. It is always associated with high serum leptin.
erythropoietin hormone secretion, and blunt the erythroid pre- In addition, its excess tends to raise tissue sodium levels while cursor response to the hormone.2 lowering tissue potassium levels. High sodium level subsequent- ly results in water retention. Low potassium results in hypogly- Moreover, lipocalin 2, an iron binding protein is pro- cemia and sweet cravings.6 duced by adipose tissue and could lead to sequestration of iron stores making them unavailable for hemoglobin or myoglobin CHROMIUM formation. Over-secretion of these proteins (hepcidin and lipo- calin 2) leads to increased iron content in adipose tissue, thus Chromium is considered an essential ultra-trace metal.
preconditions for adverse effects of local iron overload; as iron Once absorbed from intestines, it is distributed to various or- is capable of inducing oxidative stress, inflammation and adi- gans of the body, especially the kidney, muscle, and liver. The pose tissue endocrine dysfunction. Thus, obesity is associated principal carrier protein is transferrin, which plays a critical with both elevated body iron stores and iron deficiency. Resul- role in the movement of chromium from blood to Low-molec- tant iron deficiency and anemia may impair mitochondrial and ular-weight chromium (LMWCr); oligopeptide low-molecular cellular energy homeostasis and further increase fatigue of obese weight (LMW) chromium (LMWCr)-binding substance (MW subjects.2 ~1,500 Da). Thereby amplifies the intracellular insulin signal.
Therefore, chromium is an active factor in the substance; Glu- ZINC cose Tolerance Factor (GTF). It enhances the tyrosine kinase ac- tivity of the insulin receptor and, which makes insulin more ef- It is an important element in DNA synthesis, gene ex- fective. Thereby controlling carbohydrate and lipid metabolism.
pression and activity of various enzymes and maintenance of Its deficiency is associated with high level of pro-inflammatory normal growth. It plays a critical role in integrity of the immune cytokines as Tumor necrosis factor alpha, Interleukin 6 and C- system and wound healing. It is also found to enhance synthesis, reactive protein (TNF-α, IL-6 and CRP), high lipids levels and storage and release of insulin. Zinc deficiency has been reported oxidative stress. However, Chromium supplementation cannot in obese subjects. However, the exact mechanism is unclear. It reverse diabetes if occurred, but it inhibits glycation process may be due to Zinc accumulation in the adipose tissue, as re- which is responsible for many of diabetes complications.6 sult of increased production of adipokines, increased Leptin production. They induce chronic inflammation and expression Factors affecting chromium deficiency; include ad- of metallothioein and Zinc-Copper transporter in hepatocytes.
vanced age, diet rich in fat, milk and other high phosphorus These proteins result in accumulation of these metals in hepa- foods tend to bind chromium to make chromium phosphates 3 7 tocytes and adipose tissue and decreased serum concentration.3 which are not absorbed through the intestines.7 Decreased serum Zinc concentration in obese patients plays a role in insulin resistance.
SELENIUM COPPER It is an essential trace element and is a key component of several selenoproteins required for normal health as Gluta- Most of absorbed dietary copper is transported to hepa- thione peroxidase. It plays an important role as an anti-oxidant, tocytes, which utilize it for their metabolism as respiration due especially when combined with vitamin E. It is also essential for to its role in cytochrome oxidase function at the mitochondrial thyroid function and regulation of the immune system.
electron transport chain and free-radical defense being anti- oxidant. Serum Copper levels were reported to be significantly Selenium is generally well absorbed in the intestines; higher in obese patients compared to normal body weight con- mostly in duodenum; some in the jejunum and ileum. Absorp- trols. Some authors reported a negative correlation between se- tion is enhanced by the presence of other antioxidants, such as rum Copper and High-density lipoprotein (HDL)-cholesterol.4 vitamins E and C. After absorption, it is transported by Low Density Lipoproteins and Very Low Density Lipoproteins (LDL The mechanism for its elevation in obese patients is un- and VLDL), where it is stored in muscle, as well as in other or- clear but it is thought to be due to pro-inflammatory cytokines gans, as the liver, kidney, and pancreas.8 released from adipose tissue as IL-1 enhance intra-cellular Zinc accumulation with intra-cellular Copper efflux, and when re- It has been reported that serum selenium is signifi- leased to blood it binds to Ceruloplasmin. High serum copper cantly lower in obese patients. Its deficiency is associated with increased oxidative stress and impaired thyroid function; since tion of chromium picolinate with time after entering the blood- type I iodothyronine 5’-deiodinase is a selenium containing en- stream. J Inorg Biochem. 2003; 94: 86-93. doi: 10.1016/S0162- zyme. This enzyme is essential for production of active thyroid 0134(02)00623-2 hormone tri-iodothyronine. However, the exact mechanism of its deficiency in obese patients is unclear; it may be due to de- 8. Rayman MP. Selenium and human health. Lancet. 2012; creased anti-oxidants. Also dietary antioxidants enhance seleni- 379(9822): 1256-1268. doi: 10.1016/S0140-6736(11)61452-9 um absorption. In addition, they are critical for maintaining and replenishing the overall antioxidant capacity of the body.9 9. Hawkes WC, Keim NL. Dietary selenium intake modulates thyroid hormone and energy metabolism in men. J Nutr. 2003; Its deficiency is associated with increased risk of infec- 133(11): 3443-3448.
tion, atherosclerosis cardiomyopathy and myopathy, also thyroid fibrosis and irreversible hypothyroidism, if Se deficiency limits peroxide destruction by the protective action of Glutathione per- oxidase.8 In conclusion; the bioavailability of trace elements may be disturbed in obese patients, and the exact prevalence of this alteration is still unknown. Deficiency of Serum Magnesium and Copper are inversely related to body weight and Body Mass In- dex (BMI). Disturbance of trace elements are associated with metabolic syndrome.6 Dietary supplementation is not the solu- tion; also bariatric surgery may aggravate the deficiency in some conditions. Controlled weight reduction should be considered with extreme care.