An important endocrine gland in the lower neck region, the thyroid is shaped like a butterfly. The trachea's front and sides contain it, while the larynx is positioned above it. In addition to being crucial for the metabolism of calcium, Additionally, it influences how the basal metabolic rate (BMR) is regulated and fosters both mental and physical development [1] . There is an isthmus, an intermediary structure, that connects the gland's two lobes—the left and right lobes. An occasional protrusion from the isthmus is the pyramidal lobe, a third lobe. From the hyoid body to the isthmus, there is a fibrous/fibromuscular band known as the levator glandulae thyroideae [2] It generates and secretes three distinct types of hormones: T4, T3, and Calcitonin. These hormones consist of an ether bond (inner ring) joining a tyrosine molecule to an outer ring called the phenyl ring [3] . The most common autoimmune disease in humans is autoimmune thyroid disease (AITD). Hashimoto's thyroiditis (HT) and Graves' disease (GD) are the two main clinical symptoms of AITD. AITD is characterized by lymphocytic infiltration of the thyroid gland. Thyroid antibodies that cause hyperthyroidism by activating the thyrotropin receptor (TSHR) on thyrocytes might cause thyroid hyperplasia as a result of this infiltration; alternatively, it can cause damage to follicular cells, destroy the thyroid gland, and cause hypothyroidism (in HT) [4].Hashimoto thyroiditis is brought on by immune processes that destroy thyroid cells through the action of cells and antibodies. In wealthy countries, The most common reason for hypothyroidism is this. On the other side, the main cause of hypothyroidism worldwide is a diet deficient in iodine. The most typical test results include low levels of free thyroxine (fT4) and excess thyroid-stimulating hormone (TSH), together with high antithyroid peroxidase (TPO) antibodies. However, patients may present with symptoms, indications, and test results comparable to hyperthyroidism in the early stages of the condition. This is because there's a chance that thyroid gland cell death occurs occasionally [5]. Graves' autoimmune disease, is most common and is caused by autoantibodies in the bloodstream called Thyroid stimulating immunoglobulins (TSIs), which are directed against the thyroid gland's TSH receptors. These autoantibodies attach to TSH receptors (TSHRs) and replicate the effects of pituitary TSH by stimulating thyroid development and function. It's quite likely that autoimmunity against thyroid tissue developed into the antibodies that cause hyperthyroidism. Eyeball protrusion affects most hyperthyroidism sufferers to some extent. Ophthalmopathy, also known as Graves' orbitopathy, is a disorder marked by edema, upper eyelid retraction, and swelling in the soft tissue surrounding the orbit of the eye [6] .Clinically shown as non-autoimmune hypothyroidism or destructive thyroiditis.Destructive thyroiditis was the diagnosis made for patients who acquired clinical Thyroid disease TD, which is characterized by an initial hyperthyroid phase followed by a progressive remission (sometimes with a hypothyroid phase) when thyroid antibodies are not present [7] .Lipids are biological substances that are frequently soluble in organic solvents and hydrophobic by nature. They play a crucial function in communication between cells and in the metabolism of the body. They are elements of the cell membrane structure [8]. Triglycerides (TGs), cholesterol, phospholipids, fatty acids, cholesterol, and other substances can all be considered forms of lipids. Since they are insoluble in plasma, lipoproteins—which differ in size, shape, and density—are used to carry them [9] . In addition to the suggested central interaction, thyroid hormones and leptin may also have a peripheral association, however this effect is unknown. Because the reduction in thermogenesis caused by fasting is linked to both thyroxine and triiodothyronine, thyroid hormones and leptin may be involved in adaptive thermogenesis via producing heat through mitochondrial uncoupling proteins [10]. Studies on leptin in humans and rodents have not consistently shown a connection between serum leptin concentrations and thyroid function. However, given that thyroid hormone plays a part in thermogenesis and the control of uncoupling proteins, leptin may play a significant role in thyroid pathophysiology [11].

Study case and Subjects

The study included (250) blood samples from femal, their ages ranged between (20-60) years. These samples involved healthy individuals and patients with hyperthyroidism and hypothyroidism the diagnosis depending on clinical symptoms and hormonal diagnosis of thyroid function tests (T4, T3 and TSH), and were divided into three groups: Control group:,  non-immune and  Autoimmune thyroid disease   (Graves and Hashemito) 

Biochemical assays

The leptin concentration in human serum was determined using the enzyme-linked immunosorbent (ELESA) technique, while the lipid level (triglycerides, cholesterol, high density lipoprotein HDL, low density lipoprotein LDL, and very density lipoprotein VLDL) was measured manually. 

Blood collection

Collection of the samples After 5 ml of pink blood was extracted, it was put in tubes devoid of coagulant (Gel tub) and allowed to freeze at room temperature.. A centrifuge was then used to separate it after that. It was then put in special tubes meant to keep samples in the refrigerator at 20 C0 for 10 minutes during 3000 cycles.

Statistical analysis

Word 2016 was used to compose the research for this study, while SPSS was used to perform the statistical analysis. The data was expressed using an arithmetic mean value, and both applications were executed on the Windows operating system.

The Nonimmune - Autoimmune hypothyroid group's for lipid profile level ( total Cholesteol ,triglyceride ,hight density lipoprotein , low density lipoprotein , very low density lipoprotein)   mean was (253±2.13)  and (227.2±4.1 ), (187.2±4.20) and (179.2±3.04) ,( 54.94±1.39) and (42.2±2.08), (160.6±2.73) and (149.4±4.65),( 37.45±0.84) and (35.86±0.61) respectively. While  the Nonmmune - Autoimmune hyper thyroid group's was (127.1±2.6) and (171.4±2.49) , (84.6±5.95) and(99.51±2.80), (26.17±1.86) and (72.35±2.36),( 83.55±4.54) and (79.17±3.67),( 16.93±1.19) and (19.9±0.56) respectively compare with control group's was (150.9 ± 2.24),( 114.72±2.64),( 32.39±1.52) ,( 95.59±2.74) and (22.94±0.53) respectively , (all data reported in mg/dl). leptin levels across different groups is provided which reached (18.79 ± 0.72) , (25.64 ± 4.77) ,  (7.91±0.51) and (11.62±0.87) in women with Non and Autoimmune hypothyroidism , Non-Autoimmune hyperthyroidism  respectively, compared with the control group, which reached (5.89±0.51)  A statistically significant mean difference between the study groups was indicated by a P < 0.001 value.as seen in table1.When comparing the Non-immune-autoimmune hypothyroid group to the control group, the results reveal a substantial rise in all lipid profile parameters (TC, TG, HDL-c, LDL-c, and VLDL-c) at (P ≤0.001). As observed in table (1), the results for the Autoimmune Hyperthyroid group at (P ≤0.01) indicate a substantial increase in TC and HDL-c, whereas the Non immune – Autoimmune Hyperthyroid group shows a significant decrease in (TC, TG, LDL-c, and VLDL-c). the current study are consistent with the [12] . Lipid metabolism is one of the key metabolic signaling pathways that is affected by thyroid hormones. These hormones have an impact on lipid breakdown, metabolism, and composition; however, disintegration is more impacted than composition. The liver is thought to be the primary organ for producing cholesterol, and TH controls the synthesis of cholesterol in the liver through a number of processes. Also referred to as HMGCR or HMG-Co A, 3-Hydroxy-3-Methyl-Glutaryl Coenzyme A Reductase is the rate-limiting enzyme, is stimulated by THs and is in charge of the production of cholesterol [13]. They also lower cholesterol by protecting the enzyme cholesterol 7-hydroxylase (CYP7A1), which converts cholesterol to bile acids, and by improving the route that eliminates cholesterol. Maintaining the right ratio of cholesterol in the body requires bile acids [14]. Hepatic lipase (HL), lipoprotein lipase (LPL), and cholesterol ester transfer protein (CETP) are all stimulated by THs. Additionally, they stop LDL from oxidizing [15] . THs control the LPL, which gets rid of the TG in chylomicron and VLDL-c molecules. It causes TG to change into non-esterified fatty acid, which is subsequently carried to the AT and kept there after re-esterification [16] . HDL levels are decreased as a result of the exchange of TG from these lipoproteins to HDL2 through CETP and the transfer of cholesterol ester from HDL2 to the lipoproteins (VLDL-c, intermediate LDL-c (IDL), and remnants). HL hydrolyzes the TG in HDL2 molecules to produce HDL3. Additionally, it transforms IDL into LDL-c and, in the end, tiny density LDL. Hypothyroid patients would have these enzymes absent from their bloodstream, whereas hyperthyroid patients would have elevated levels of them [17] By binding to SREBP, T3 promotes the creation of LDL-c receptors and the regulatory enzymes involved in the synthesis of cholesterol. If there were no THs, blood levels of LDL-c would increase. Thus, because hypothyroidism reduces the expression of LDL receptors (LDLr), it results in hypercholesterolemia [18] . causing an imbalance in the uptake of cholesterol, which in turn causes a marked rise in the levels of Apo lipoprotein B (Apo B), TC, and LDL-c as well as a reduction in the blood's clearance of TC and LDL-c. Furthermore, a decrease in LPL activity is responsible for a decrease in the clearance of TG levels in circulation as well as the aggregation of IDL. On the other hand, hyperthyroidism causes this to occur. An excess of THs increases the activity of these enzymes, decreases blood levels of TC and TG due to improved removal via reverse cholesterol transport (RCT) signaling, and increases β-oxidation in the liver due to lipolysis in the AT [19]. Our results are in line with the study [20], which found that the hypothyroid patients' HDL-c values were significantly lower than those of the control group. Patients with hypothyroidism had a larger ratio of LDL-c to HDL-c, which raised their risk of cardiovascular disease due to an increase in LDL-c and a slight decline in HDL-c levels. But as was already mentioned, THs impact LDL receptor expression and LPL activity in nonimmune hyperthyroidism. Additionally, they affect the metabolism of HDL-c by increasing the activity of CEPT, which changes HDL-c into VLDL-c. This could account for our study's findings of decreased HDL-c levels [21] . Additionally, T3 has been linked to preventing LDL-c from oxidizing to become oxidized LDL-c . This increases the likelihood of thrombus formation by causing endothelial cell absorption and the production of inflammatory activity. The inflammation makes the plaque fragile, and when it ruptures, a thrombus develops [22-24] . 

Table 1: Compare lipid profile level in serum  of women with thyroid disease for different group

the levels of leptin in hypothyroid patients were higher than in hyperthyroid patient, and this is consistent with [25,26] ,their results explain that energy storage and food intake are significantly regulated by TSH and THs. In thermogenesis, the balance between lipogenesis and lipolysis, and adipogenesis, they have regulatory functions. Chronic low-grade inflammation may be brought on by elevated TSH. They have regulatory functions in adipogenesis, thermogenesis, and the balance between lipogenesis and lipolysis. A high TSH level could lead to low-grade persistent inflammation. It is well recognized that slight fluctuations in thyroid function are closely associated with changes in body weight, and that adipose tissue influences thyroid function through a variety of methods. There are three factors: adipocytokine release, lipotoxicity, and chronic inflammation. Even a slow thyroid dysfunction in humans can lead to an increase in body mass and fat, and in obese patients, a slightly increased TSH could be a sign of subclinical hypothyroidism. Interpreting TSH tests requires determining the reason of hypothyroidism. It is conceivable, therefore, that activation of the hypothalamic-pituitary-thyroid axis could lead to hyperthyrotropinemia. The differentiation of reasons of increased TSH levels may be aided by measuring the concentration of fT3. It is hypothesized that obesity, an inflammatory condition, and lipotoxicity could result in thyroid gland dysfunction; so, encouraging weight loss by dietary and lifestyle modifications is required to impede adverse events. The current study's findings demonstrated that patients with Autoimmune hypothyroidism (HT ) had higher serum leptin levels than Autoimmune hyperthyroidism (GD ) patients. There have been no consistent findings from human investigations on the relationship between serum leptin levels and thyroid function. Certain research [27], found that patients with hypothyroidism had higher serum leptin levels, however other investigations[28] , found lower levels in these patients. Additionally, a few studies found no differences between the hypothyroid and euthyroid patients in the control group [29,30] . Furthermore, it is unclear why the findings of earlier research are inconsistent and occasionally contradicting. Autoimmunity, leptin pulsatility, leptin-binding proteins, sex, fertility status, differences in the study populations' characteristics, autoimmune or nonautoimmune causes of thyroid dysfunction, treatment exposure or nonexposure, duration of treatment, and different leptin assay measurement techniques are just a few of the variables that could be involved. Thus, it is reasonable to expect different results from different studies. As such, it is realistic to anticipate that various investigations may yield different findings. This study is similar to a cross-sectional study carried out by [26] In this study, we made an effort to offer a sufficiently large sample of individuals who are newly diagnosed with autoimmune hypo- and hyperthyroidism but are not yet receiving treatment. Moreover, only the age distribution of the groups was matched. The current study did, however, have certain shortcomings. The follow-up period with patients lasted a mere three months. Perhaps there would have been more noticeable variations in serum leptin levels before and after therapy if the patients had been monitored for longer lengths of time following their euthyroidism.

The authors declare that they have no conflict of interest

No funding sources

The study was approved by the University of Kirkuk, Kirkuk, Iraq.

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