90
pathogenesis of PCOS. Further, obesity and hypertension exacerbate the underlying
metabolic syndrome. Additionally, PCOS is further involved in the pathogenesis of
cancer, obstructive sleep apnea, diabetes, and psychological problems like depression [52].
Alternatively, the primary symptoms associated with PCOS are dermatological
signs (alopecia, hirsutism, and acne) along with the abnormal menses. In addition to
these, biochemical alterations linked with elevated testosterone level and increased
pituitary LH release are the consequences of insulin resistance and subsequent
hyperinsulinemia. Likewise, hyperandrogenism in conjugation with elevated LH
level leads to disturbance in physiological process related to ovarian follicular maturation and finally gives to anovulatory cycles [48]. In fact, dyslipidemia is considered to play a key role in the incidence and prevalence of PCOS. Thus, lipid
abnormalities are accompanied by increased low-density lipoprotein (VLDL) and
triglycerides (TGs), while diminished high density lipoproteins (HDL) are often
seen in women with PCOS. Subsequently, such women have increased waist to hip
ratio [53]. In addition to this, one pilot study has also demonstrated that women having PCOS exhibits reduced capability of switching during the overnight fasting
along with daily metabolism from glucose to lipid oxidation [50]. It is known that
polyunsaturated fatty acids (PUFAs) and their ultimate derivatives have fundamental contribution in the dissemination of PCOS. This is evident from abnormal level
of FFAs, PUFAs metabolites, and phosphatidylcholine in women with PCOS [51].
Finally discussing all the pathogenesis and ultimate consequences of PCOS,
there is a fundamental need for the pharmacological and non-pharmacological interventions for tackling PCOS. Non-pharmacological interventions include life-style
management such as weight reduction, maintaining BMI which diminishes insulin
resistance and subsequently improves insulin sensitivity, leading towards protective
effect on metabolic and reproductive features. Additionally, proper counseling and
nutritional supplements like inositol and N-acetylcysteine has also shown beneficial
outcomes [54]. Coming towards pharmacological treatments, drugs that improve
lipid profile are better therapeutic targets for PCOS. Such as metformin reduces
body weight, FSH and glucose levels as well as androgen. It is utilized for the treatment of PCOS [11]. So, we can summarize that strategies must be adopted for
subsiding or mitigating the incidence and progression of PCOS and its ultimate
consequences.
Impaired Lipid Metabolism and Neuroinflammation
As brain development is a sequenced process usually accomplished by the unique/
particular well-defined stages regarding growth and maturation. Among these,
one of the pivotal events is formation of myelin sheath. Dietary lipids have an
influential role in this process [55]. Recently, a study in male rats interprets that
high fat diet ingestion for nine weeks induces obesity and also affects incidence
and dissemination of neuroinflammation. This neuroinflammatory response was
K. Haider et al.
pathogenesis of PCOS. Further, obesity and hypertension exacerbate the underlying
metabolic syndrome. Additionally, PCOS is further involved in the pathogenesis of
cancer, obstructive sleep apnea, diabetes, and psychological problems like depression [52].
Alternatively, the primary symptoms associated with PCOS are dermatological
signs (alopecia, hirsutism, and acne) along with the abnormal menses. In addition to
these, biochemical alterations linked with elevated testosterone level and increased
pituitary LH release are the consequences of insulin resistance and subsequent
hyperinsulinemia. Likewise, hyperandrogenism in conjugation with elevated LH
level leads to disturbance in physiological process related to ovarian follicular maturation and finally gives to anovulatory cycles [48]. In fact, dyslipidemia is considered to play a key role in the incidence and prevalence of PCOS. Thus, lipid
abnormalities are accompanied by increased low-density lipoprotein (VLDL) and
triglycerides (TGs), while diminished high density lipoproteins (HDL) are often
seen in women with PCOS. Subsequently, such women have increased waist to hip
ratio [53]. In addition to this, one pilot study has also demonstrated that women having PCOS exhibits reduced capability of switching during the overnight fasting
along with daily metabolism from glucose to lipid oxidation [50]. It is known that
polyunsaturated fatty acids (PUFAs) and their ultimate derivatives have fundamental contribution in the dissemination of PCOS. This is evident from abnormal level
of FFAs, PUFAs metabolites, and phosphatidylcholine in women with PCOS [51].
Finally discussing all the pathogenesis and ultimate consequences of PCOS,
there is a fundamental need for the pharmacological and non-pharmacological interventions for tackling PCOS. Non-pharmacological interventions include life-style
management such as weight reduction, maintaining BMI which diminishes insulin
resistance and subsequently improves insulin sensitivity, leading towards protective
effect on metabolic and reproductive features. Additionally, proper counseling and
nutritional supplements like inositol and N-acetylcysteine has also shown beneficial
outcomes [54]. Coming towards pharmacological treatments, drugs that improve
lipid profile are better therapeutic targets for PCOS. Such as metformin reduces
body weight, FSH and glucose levels as well as androgen. It is utilized for the treatment of PCOS [11]. So, we can summarize that strategies must be adopted for
subsiding or mitigating the incidence and progression of PCOS and its ultimate
consequences.
Impaired Lipid Metabolism and Neuroinflammation
As brain development is a sequenced process usually accomplished by the unique/
particular well-defined stages regarding growth and maturation. Among these,
one of the pivotal events is formation of myelin sheath. Dietary lipids have an
influential role in this process [55]. Recently, a study in male rats interprets that
high fat diet ingestion for nine weeks induces obesity and also affects incidence
and dissemination of neuroinflammation. This neuroinflammatory response was
K. Haider et al.