In recent years, breast cancer is one of the most common malignancies among women, with the increasing occurrence [
1]. For premenopausal breast cancer patients, included are such treatment strategies as surgery, cytotoxic chemotherapy, endocrine therapy, radiation therapy, and targeted therapy
2, which, despite the improved survival rates, may have side effects such as early menopause and fertility disorders [
2]. Based on a meta-analysis, the pregnancy probability of women receiving systemic treatment after surgery is about 14%, and the pregnancy rate of the survivors after receiving breast cancer treatment is on average 40% lower compared with general female [
3], leaving many female patients concerned about infertility in the future and early menopausal symptoms [
4]. The fertility preservation can be assessed with ovarian reserve biomarkers such as anti-müllerian hormone (AMH), inhibin B levels, antral follicle count (AFC), early follicular phase follicle stimulating hormone (FSH), and estradiol [
5]. The recruitment of primitive follicles and the effect of FSH on follicles during growth can be inhibited by AMH, a glycoprotein hormone in the transforming growth factor-beta (TGF-β) family [
6], which is supported by Ruddy et al. that with aging, the risks of amenorrhea at 12 months and 18 months after chemotherapy increase by 20% and 18% respectively, while with each 1 ng/mL increase in AMH, the chance of amenorrhea at the 18th month of chemotherapy decreases by 59%[
7]. Nowadays, AMH has been shown, in young premenopausal women with breast cancer, to be the most sensitive marker for predicting ovarian function recovery and premature ovarian insufficiency [
8]. The purpose of this review is to discuss whether there is a correlation between AMH and fertility in young patients with breast cancer, thus guiding the selection of fertility protection strategies, with the association between metabolism and AMH examined to assess the impact of metabolism on fertility.