Background: Somatotropic axis dysfunction associated with non-alcoholic fatty liver disease (NAFLD) has potential multisystemic detrimental effects. Here, we analysed the effects of growth hormone (GH) and insulin-like growth factor-1 (IGF-1) supplementation on liver histology, adipokine profile and muscle function in an NAFLD model. Methods: C57BL/6 mice were fed with a high fat diet (HFD) for 12 weeks and were separated into three groups treated for 4 weeks with: (1) High fat diet (HFD) (n = 10); (2) HFD + GH 9 μg/g/d (n = 10); (3) HFD + IGF-1 0.02 µg/g/d (n = 9). A control group fed a chow diet was included (n = 6). Liver histology, liver triglycerides content, serum alanine aminotransferase (ALT) activity, adiponectin and leptin serum levels, in vivo muscle strength, tetanic force and muscle fibre cross-sectional area (CSA) were measured. Results: HFD + GH and HFD + IGF-1 groups showed significantly lower ALT activity compared to HFD (p < 0.01). Liver triglyceride content in HFD + GH was decreased compared to HFD (p < 0.01). Histologic steatosis score was increased in HFD and HFD + GH group (p < 0.01), whereas HFD + IGF-1 presented no difference compared to the chow group (p = 0.3). HFD + GH group presented lower serum leptin and adiponectin levels compared to HFD. GH and IGF-1 supplementation therapy reverted HFD-induced reduction in muscle strength and CSA (sarcopenia). Conclusions: GH and IGF-1 supplementation induced significant improvement in liver steatosis, aminotransferases and sarcopenia in a diet-induced NAFLD model.

Prostate cancer (PCa) is the second leading cause of cancer-related death among men in most Western countries. Current therapies for PCa are limited, often ineffective, and associated with significant side effects. As a result, there is a growing interest in exploring new therapeutic agents, particularly from the polyphyletic group of algae, which offers a promising source of compounds with anticancer properties. Our research group has focused on investigating the effects of a novel oleoresin from Gracilaria chilensis, known as Gracilex^®, as a potential therapeutic agent against PCa using both in vitro and in vivo models. Our findings indicate that Gracilex^® exhibits a time- and dose-dependent inhibitory effect on cell survival in LNCaP and PC-3 PCa, reducing viability by over 50% and inducing apoptosis, as evidenced by a significant increase in activated caspase-3 expression in both cell lines. Moreover, Gracilex^® significantly reduces the proliferation rate of both LNCaP and PC-3 prostate cancer cell lines, as evidenced by a marked decrease in the growth curve slope (p = 0.0034 for LNCaP; p < 0.0001 for PC-3) and a 40–50% reduction in the proportion of Ki-67-positive PCa cells. In addition, Gracilex^® significantly reduces in vitro cell migration and invasion in LNCaP and PC-3 cell lines. Lastly, Gracilex^® inhibits tumor growth in an in vivo xenograft model, an effect that correlates with the reduced PCa cell proliferation observed in tumor tissue sections. Collectively, our data strongly support the broad antitumoral effects of Gracilex^® on PCa cells in vitro and in vivo. These findings advance our understanding of its potential therapeutic role in PCa and highlight the relevance of further investigating algae-derived compounds for cancer treatment.

Metabolic dysfunction-associated steatotic liver disease (MASLD)-related hepatocarcinogenesis involves metabolic injury, fibrosis, and dysregulated regenerative signaling. Because growth hormone (GH) and insulin-like growth factor 1 (IGF-1) can support repair but also activate proliferative pathways, their effects in advanced disease remain uncertain. We investigated that effect in a MASLD-related HCC model. Male C57BL/6J mice received a Western Diet (WD) and weekly carbon tetrachloride (CCl₄) injections for 24 weeks. At week 16, mice were allocated to untreated or hormone-treated groups, with continuous subcutaneous infusion of IGF-1 at 20 or 60 µg/kg/day or GH at 0.5 or 2 mg/kg/day for 8 weeks. Both hormones reduced serum aminotransferases, lobular inflammation, hepatic collagen and altered selected fibrosis-related transcripts, whereas to IGF-1 20 µg/kg/day and GH 2 mg/kg/day reduced steatosis, and IGF-1 20 µg/kg/day and GH 0.5 mg/kg/day reduced hepatocyte ballooning. GH at 2 mg/kg/day was associated with fewer macroscopically detected hepatic surface nodules, while IGF-1 did not alter nodule burden. The GH 2 mg/kg/day group also showed a lower hepatic p-ERK/ERK ratio. Thus, continuous GH administration during late-stage WD/CCl₄-induced hepatocarcinogenesis was associated with lower hepatic nodule burden. Histopathological confirmation of the lesions and validation in additional models are required before interpreting this finding as an antitumor or therapeutic effect.