Thus, obesity is associated with hyperleptinemia
and leptin resistance .
However, in cases of obesity-associated hyperleptinemia
, this vasodilatory effect is lost with subsequent development of hypertension.
The HFD also promoted many indicators that resemble those of human comorbidities caused by obesity, such as hyperinsulinemia, hyperleptinemia
, and elevated serum GL, T-Chol, and TG levels.
Thus, it is hard to explain why neurodegeneration is increased in patients suffering from MS, since the condition usually causes hyperleptinemia
. This may be partially explained by resistance to this hormone in peripheral tissues, causing augmented secretion of this peptide as well as diminished leptin transport across the BBB .
Nevertheless, further studies should be conducted in the mare to better understand the response mechanisms to euleptinemia and hyperleptinemia
Given that levels of the hormone leptin are normally increased during pregnancy, the authors propose that future research should seek to determine whether BPA directly regulates leptin release from fatty tissue or whether the observed hyperleptinemia
is a consequence of the altered metabolic state of these animals.
rapidly depletes adipocyte fat in lean rats, whereas comparable hyperleptinemia
produced by adipocytes in diet-induced obesity does not, implying a leptinergic blockade in adipocytes during overnutrition.
is an essential feature of human obesity.
The significance of hyperleptinemia
in breast, colorectal, and hepatocellular cancer has been well documented , and some studies suggest the role of leptin in thyroid cancerogenesis .
It has been postulated that, in obesity, neurons located in the ventromedial hypothalamic nucleus that express leptin receptors become desensitized to chronically elevated levels of leptin (hyperleptinemia
) suppressing its anorexigenic effects while selectively preserving sympathoexcitation (known as "selective leptin resistance") [57, 58].
Furthermore, dysregulated metabolic parameters such as hyperglycemia, hyperlipidemia, and hyperleptinemia
are important contributors and amplifiers of systemic oxidative stress (Figure 3).
The HFD model is extremely efficient for creating pathophysiological conditions such as hyperleptinemia
, peripheral insulin resistance, diabetes mellitus, and obesity that lead to long-term metabolic and energy disorders.