Excess caloric intake can lead to insulin resistance. The underlying reasons are complex but likely related to ectopic lipid deposition in nonadipose tissue. We hypothesized that the inability to appropriately expand subcutaneous adipose tissue may be an underlying reason for insulin resistance and beta cell failure. Mice lacking leptin while overexpressing adiponectin showed normalized glucose and insulin levels and dramatically improved glucose as well as positively affected serum triglyceride levels. Therefore, modestly increasing the levels of circulating full-length adiponectin completely rescued the diabetic phenotype in ob/ob mice. They displayed increased expression of PPARgamma target genes and a reduction in macrophage infiltration in adipose tissue and systemic inflammation. As a result, the transgenic mice were morbidly obese, with significantly higher levels of adipose tissue than their ob/ob littermates, leading to an interesting dichotomy of increased fat mass associated with improvement in insulin sensitivity. Based on these data, we propose that adiponectin acts as a peripheral "starvation" signal promoting the storage of triglycerides preferentially in adipose tissue. As a consequence, reduced triglyceride levels in the liver and muscle convey improved systemic insulin sensitivity. These mice therefore represent what we believe is a novel model of morbid obesity associated with an improved metabolic profile.

/pdf/obesity-associated-improvements-in-metabolic-profile-through-1gz4ukej0v.pdf

Obesity-associated improvements in metabolic profile through expansion of adipose tissue

Consensus on infertility treatment related to polycystic ovary syndrome

Idiopathic intracranial hypertension is common in obese women and can lead to significant visual impairment. First described more than 100 years ago, the cause of the disorder remains unknown. Despite a multitude of proposed links, the aetiology has never been established. Impairment of cerebrospinal-fluid reabsorption is the most likely underlying pathophysiological cause of the raised pressure, but this notion has yet to be proven. Cerebral venous sinus abnormalities associated with the disorder need further exploration. Although the major symptoms of headache and visual disturbance are well documented, most data for disease outcome have been from small retrospective case series. No randomised controlled trials of treatment have been done and the management is controversial. The importance of weight loss needs clarification, the role of diuretics is uncertain, and which surgical intervention is the most effective and safe is unknown. Prospective trials to examine these issues are urgently needed.

https://www.thelancet.com/pdfs/journals/laneur/PIIS1474-4422(06)70442-2.pdf

Idiopathic intracranial hypertension

Whilst many multiparous women are obese (body mass index >30 kg/m(2)), obesity has been associated with impaired fecundity; however, the mechanism which links obesity to reduced fertility remains to be fully elucidated. Obese women, particularly those with central obesity, are less likely to conceive per cycle. Obese women suffer perturbations to the hypothalamic-pituitary-ovarian axis, menstrual cycle disturbance and are up to three times more likely to suffer oligo-/anovulation. A fine hormonal balance regulates follicular development and oocyte maturation, and it has been observed that obesity can alter the hormonal milieu. Leptin, a hormone produced by adipocytes, is elevated in obese women, and raised leptin has been associated with impaired fecundity. Obesity impairs ovulation but has also been observed to detrimentally affect endometrial development and implantation. The expression of polycystic ovary syndrome (PCOS) is regulated, in part, by weight, and so obese women with PCOS often have a more severe phenotype and experience more subfertility. Obesity also impairs the response of women to assisted conception treatments. Weight loss through lifestyle modification or bariatric surgery has been demonstrated to restore menstrual cyclicity and ovulation and improve the likelihood of conception. In this article, we will discuss the effect of obesity upon key reproductive mechanisms and its relation to fertility treatments.

/pdf/the-adverse-effects-of-obesity-on-conception-and-1i68nbv55n.pdf

The adverse effects of obesity on conception and implantation

https://www.fertstert.org/article/S0015-0282(03)02846-2/pdf

Negative lifestyle is associated with a significant reduction in fecundity.

The recent discovery of the obese (ob) gene has provided new insight into the mechanism which controls body fat mass. Leptin, a product of the ob gene, serves as the link between fat and the brain. This protein, by acting at the level of the hypothalamus, decreases food intake and increases energy expenditure. Animals that lack leptin (ob/ob mice) develop profound obesity and become infertile. Treatment of these animals with leptin reduces food intake and restores normal fertility. Although leptin is important for the control of fat stores in certain species, the role of this substance in the development of human obesity remains obscure. However, it has been speculated that, in humans, obesity is related to leptin resistance. The relationship between fat and reproduction has been recognized for >20 years. This article discusses the relationship between leptin and human reproduction. In particular, recent knowledge about the possible role of leptin in various conditions such as puberty, polycystic ovary syndrome and pregnancy is reviewed. Also, the article discusses the possible role of leptin in ovarian function and the relationship of this protein with gonadal steroids. It is expected that future research will clarify the physiological importance of leptin in human reproductive function.

/pdf/leptin-in-human-reproduction-4qemvclyru.pdf

Leptin in human reproduction

To study the relationships between gonadal steroids and leptin, 20 women with normal cycles were investigated during the postoperative period following a laparotomy. Fourteen women underwent bilateral ovariectomy plus total hysterectomy either in the mid- to late follicular phase (n = 7, group 1) or in the early to midluteal phase (n = 7, group 2). The remaining six of the 20 women underwent cholocystectomy in the early to midfollicular phase of the cycle and were used as controls (group 3). In all three groups, serum leptin values decreased rapidly up to post-operative day 4. Then, leptin values increased significantly only in group 3 (P < 0.05). Leptin values before and after the operation showed significant positive correlations with body mass index (BMI), oestradiol and progesterone. However, with multiple regression analysis, BMI was the only parameter significantly correlated with leptin in group 3 (days 0 and 4-7), whereas in groups 1 and 2 progesterone and BMI showed independent significant correlations with leptin (days 0 and 8, r = 0.601 and r = 0.602 respectively). These results demonstrate for the first time a significant reduction in leptin concentrations in normal women following bilateral ovariectomy. Although BMI seems to be the predominant factor, it is also suggested that oestradiol and progesterone may participate in the control of leptin production during the human menstrual cycle.

Leptin concentrations in normal women following bilateral ovariectomy

BACKGROUND: Previous studies have alluded to a role for both oestradiol and progesterone in the secretion of leptin from fat cells in the human, although direct evidence has yet to be obtained. The study aim was to assess serum leptin concentrations in normally cycling women receiving exogenous oestradiol and progesterone. METHODS: Normally cycling women were investigated in an untreated spontaneous cycle (control, n 10), a cycle treated with oestradiol (oestradiol cycle, n 10) and a cycle treated with oestradiol plus progesterone (oestradiolprogesterone cycle, n 6). Oestradiol was given to the women through skin patches on cycle days 2, 3 and 4, and progesterone intravaginally on cycle days 3, 4 and 5. Serum concentrations of leptin, oestradiol, progesterone, FSH and LH were measured in daily blood samples. RESULTS: During the treatment, serum oestradiol and progesterone concentrations increased significantly. In the oestradiol cycles, leptin concentrations were not affected by treatment and did not differ from those in controls. In the oestradiolprogesterone cycles, leptin concentrations (mean SEM) increased in all women from cycle day 3 (8.6 1.1 ng/ml) to days 5 (12.2 1.8 ng/ml, P < 0.01) and 6 (11.9 2.0, P < 0.05), and were at these points significantly higher than in the control cycles (P < 0.05). The mean percentage increase from day 3 to the peak concentration on days 5 or 6 was 62.6 6.8%. Leptin concentrations returned to the pretreatment value on day 7, together with the concentrations of oestradiol and progesterone. In the oestradiolprogesterone cycles, leptin concentrations correlated significantly with oestradiol and progesterone concentrations, but not with FSH and LH concentrations. CONCLUSIONS: These results show, for the first time, that leptin secretion can be stimulated in women by the administration of oestradiol plus progesterone. This may explain the increased concentrations of leptin during the luteal phase of the normal menstrual cycle.

/pdf/oestradiol-plus-progesterone-treatment-increases-serum-4kqzbq4ptu.pdf

Oestradiol plus progesterone treatment increases serum leptin concentrations in normal women.

Great progress had been achieved during the last 20 years in the field of ovulation induction in patients with polycystic ovary syndrome (PCOS). Clomiphene citrate remains the first line of treatment for all anovulatory women with PCOS, since in properly selected patients the cumulative pregnancy rate approaches that in normal women. Human urinary gonadotrophins have been used extensively for ovulation induction, but the development of low-dose regimens has opened a new era in the management of anovulation related to PCOS. This article discusses the main advantages and disadvantages of the principal methods and regimens currently used for ovulation induction in patients with PCOS including clomiphene citrate, gonadotrophins, pulsatile gonadotrophin-releasing hormone (GnRH) and GnRH agonists. It also discusses new drugs discovered recently, particularly recombinant gonadotrophins and GnRH antagonists, and provides some thoughts regarding their use in future protocols. Finally, based on the discovery of new ovarian substances which specifically control luteinizing hormone (LH) secretion, this article develops assumptions on possible implications of these substances in the pathophysiology of PCOS and their potential use in the management of the syndrome.

/pdf/current-and-future-status-of-ovulation-induction-in-417ej2g3tp.pdf

Current and future status of ovulation induction in polycystic ovary syndrome

(P < 0.01) and were significantly higher than in the other two groups (P < 0.05). Body mass index (BMI) was the Patients most important variable accounting for the changes in The study included 21 normally ovulating women who volunteered leptin values post-operatively, but in the oestradiol plus for the study and gave written informed consent. Approval for the progesterone group progesterone correlated significantly study was obtained from the local ethical committee. Clinical and with leptin independently of BMI. These results suggest endocrine characteristics of the women are shown in Table I. There were no significant differences in the age, body mass index (BMI), that progesterone and cortisol can stimulate leptin secretion FSH, luteinizing hormone (LH), leptin and cortisol values between in women regardless of oestradiol concentrations.

/pdf/treatment-of-normal-women-with-oestradiol-plus-progesterone-2h5pkzylno.pdf

Treatment of normal women with oestradiol plus progesterone prevents the decrease of leptin concentrations induced by ovariectomy

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