Cellulite is a connective tissue disorder seen mainly in postadolescent females. In the rare occasions that cellulite is witnessed in men, it is more common in males with androgen – deficient conditions such as hypogonadism, Klinefelter’s syndrome, and in patients receiving estrogen-based therapy for prostate cancer [14]. Furthermore, where cellulite is displayed in both obese and thin females, obese males are rarely inflicted with the condition. These findings imply that a hormonal component plays an important role in the etiology of cellulite.
Estrogens and androgens are involved in the formation of cellulite. Estrogen stimulates lipogenesis (lipid synthesis) and inhibits lipolysis (fatty acid oxidation—not synonymous
• Alters fibrous septae
• Stimulates proliferation of fibroblasts
• Controls macromolecule turnover
• Stimulates replication of adipocytes
Figure 16.4 The role of estrogen in the onset of cellulite.
with apoptosis), two adipocyte processes that are critical to the metabolic functions of adipocytes that occur throughout the life of the cell. Although the balance of lipogenesis and lipolysis varies according to gender, race, and age, it is important to note that this balance is the ultimate determinant of adipocyte volume and potential adipocyte hypertrophy [15]. Estrogens have a potent influence on the anatomical enlargement of adipocytes in women. The latter may be a reason for the onset of cellulite at puberty, as well as the proliferation of cellulite during pregnancy, estrogen therapy, and menstruation.
The onset of cellulite at menstruation and the exacerbation of cellulite with age may be due to the secretion of matrix metalloproteinases (MMPs) such as collagenase and gelati- nase. Endometrial cells must secrete these two enzymes to allow menstrual bleeding to occur. Additionally, endometrial collagenase secretion also causes dermal collagen breakdown. With extended cyclical collagenase release (and with increased age), more and more dermal collagen is torn down, explaining the worsening of cellulite observed with age [5].
The mechanism of cellulite initiation by estrogens has recently been found to be more involved than simply lipogenesis and lipolysis. Estrogen perpetuates cellulite formation by stimulating the proliferation of fibroblasts, controlling macromolecule turnover, and stimulating the replication of adipocytes. Estrogens are also responsible for altering gly – coaminoglycans (GAGs) and collagen, which aggravates fibrosclerosis in connective tissue fibrous septae [16].
However, estrogen is not the only perpetrator of cellulite formation. Other hormones, such as insulin and catecholamines stimulate or inhibit lipolysis or lipogenesis, thus altering adipocyte metabolism. Finally, thyroid hormones are known to contribute to lipolysis enhancement within the fatty tissue as well [16] (Fig. 16.4).