Obesity is a growing epidemiological problem, as two-thirds of the adult population are carrying excess weight. It is a risk factor for the development of cardiovascular diseases (hypertension, ischemic heart disease, myocardial infarct, and atrial fibrillation). It has also been shown that chronic obesity in people may be a cause for the development of heart failure with preserved ejection fraction (HFpEF), whose components include cellular hypertrophy, left ventricular diastolic dysfunction, and increased extracellular collagen deposition. Several animal models with induced obesity, via the administration of a high-fat diet, also developed increased heart fibrosis as a result of extracellular collagen accumulation. Excessive collagen deposition in the extracellular matrix (ECM) in the course of obesity may increase the stiffness of the myocardium and thereby deteriorate the heart diastolic function and facilitate the occurrence of HFpEF. In this review, we include a rationale for that process, including a discussion about possible putative factors (such as increased renin–angiotensin–aldosterone activity, sympathetic overdrive, hemodynamic alterations, hypoadiponectinemia, hyperleptinemia, and concomitant heart diseases). To address the topic clearly, we include a description of the fundamentals of ECM turnover, as well as a summary of studies assessing collagen deposition in obese individuals.

Research on proteins and peptides that play roles in metabolic regulation, which may be considered potential insulin resistance markers in some medical conditions, such as diabetes mellitus, obesity and polycystic ovarian syndrome (PCOS), has recently gained in interest. PCOS is a common endocrine disorder associated with hyperandrogenemia and failure of ovulation, which is often accompanied by metabolic abnormalities, including obesity, dyslipidemia, hyperinsulinemia, and insulin resistance. In this review, we focus on less commonly known peptides/proteins and investigate their role as potential biomarkers for insulin resistance in females affected by PCOS. We summarize studies comparing the serum fasting concentration of particular agents in PCOS individuals and healthy controls. Based on our analysis, we propose that, in the majority of studies, the levels of nesfastin-1, myonectin, omentin, neudesin were decreased in PCOS patients, while the levels of the other considered agents (e.g., preptin, gremlin-1, neuregulin-4, xenopsin-related peptide, xenin-25, and galectin-3) were increased. However, there also exist studies presenting contrary results; in particular, most data existing for lipocalin-2 are inconsistent. Therefore, further research is required to confirm those hypotheses, as well as to elucidate the involvement of these factors in PCOS-related metabolic complications.

Premature ovarian insufficiency (POI) is defined as a cessation of ovarian function before the age of 40. Such early deprivation of estrogens in women may be associated with several adverse cardiovascular and metabolic consequences. The aim of this retrospective study was to investigate whether women with POI and a serum follicle-stimulating hormone (FSH) level of 25–40 I/U (Group A) have the same metabolic profile as women with POI and a serum FSH level of >40 I/U (Group B). One hundred twenty-three women were included in the study group (Group A; n = 41; Group B; n = 82). The control group comprised 77 healthy women with regular menstruation. In the age- and BMI-adjusted model, no differences were found between the groups with respect to total cholesterol, high-density lipoproteins, triglycerides, HOMA-IR, glucose, and insulin. The only significant difference was found in terms of low-density lipoprotein cholesterol (LDL-C). The highest serum concentration was found in Group B, the second highest was found in Group A, and the lowest was in the controls. In conclusion, changing the threshold of FSH required to establish a POI diagnosis may have an impact on the level of serum LDL-C.