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Few studies have examined the distinct reproductive concerns (RC) of men and women in the adolescent and young adult (AYA) cancer patient population. The purpose of this mixed-methods study was to explore and differentiate the RC of AYAs. Participants completed the Reproductive Concerns After Cancer (RCAC) scale and participated in a semistructured interview. Interviews were deductively coded based on an analytic schema derived from the RCAC. After identifying participants through the electronic health record, 27 younger AYAs, ages 12–25, enrolled in the study. Four inductive themes emerged and differed by gender. These include differential temporality, acceptance, and openness to alternatives, partner influence, and parental/guardian influence. AYA men reported fewer RC (M = 49.4, SD = 9.6) compared to AYA women (M = 56.8, SD = 8.4). Oncofertility care providers are advised to account for short- and long-ranging concerns based on AYAs' gender. Future evaluations of patient-reported outcome measures specific to AYA RC are recommended. [ABSTRACT FROM AUTHOR]

Body image is a major psychosocial concern for all cancer patients but can affect the adolescent and young adult (AYA) population in distinct ways. Similarly, the prospect of infertility and the fertility preservation process can create additional stress during cancer treatment. Discussions regarding infertility inherently implicate the body and its reproductive function, but downstream effects on self-perception have not been previously described. The aim of this study was to explore the experiences of AYAs as they considered their risk of infertility and options for fertility preservation (FP), specifically the ways in which this impacted body image and FP decision-making. AYA cancer patients (n = 27) aged 12–25 years whose cancer and treatment conferred risk of infertility were recruited through electronic health record query at an NCI-Designated Comprehensive Cancer Center. Participants completed semi-structured interviews, which were recorded, transcribed, and deductively coded for themes related to information needs, knowledge of treatment effects on fertility, and reproductive concerns after cancer. Emergent, inductive themes related to body image were identified. Body image concerns, related to both physical appearance and body functioning emerged. Common concerns included anticipating change as it pertains to the body and its functions, physical discomfort, fear of judgment, and meeting expectations of the body. While these themes are broad in nature, they have been previously explored in relation to body image in general and their emergence in the oncofertility space provides guidance for further optimization of infertility and fertility preservation discussions. AYA cancer patients experience a multitude of body image related disturbances when faced with the possibility of infertility and fertility preservation. In identifying and exploring these themes, future opportunities for improving oncofertility practice and discussions among AYAs with a focus on body image positivity are called upon. [ABSTRACT FROM AUTHOR]

Insulin secretion from β-cells is tightly regulated by local signaling from preproglucagon (Gcg) products from neighboring α-cells. Physiological paracrine signaling within the microenvironment of the β-cell is altered after metabolic stress, such as high-fat diet or the β-cell toxin, streptozotocin (STZ). Here, we examined the role and source of Gcg peptides in β-cell function and in response to STZ-induced hyperglycemia. We used whole body Gcg null (GcgNull) mice and mice with Gcg expression either specifically within the pancreas (GcgΔPanc) or the intestine (GcgΔIntest). With lower doses of STZ exposure, insulin levels were greater and glucose levels were lower in GcgNull mice compared with wild-type mice. When Gcg was functional only in the intestine, plasma glucagon-like peptide-1 (GLP-1) levels were fully restored but these mice did not have any additional protection from STZ-induced diabetes. Pancreatic Gcg reactivation normalized the hyperglycemic response to STZ. In animals not treated with STZ, GcgNull mice had increased pancreas mass via both α- and β-cell hyperplasia and reactivation of Gcg in the intestine normalized β- but not α-cell mass, whereas pancreatic reactivation normalized both β- and α-cell mass. GcgNull and GcgDIntest mice maintained higher β-cell mass after treatment with STZ compared with control and GcgΔPanc mice. Although in vivo insulin response to glucose was normal, global lack of Gcg impaired glucose-stimulated insulin secretion in isolated islets. Congenital replacement of Gcg either in the pancreas or intestine normalized glucose-stimulated insulin secretion. Interestingly, mice that had intestinal Gcg reactivated in adulthood had impaired insulin response to KCl. We surmise that the expansion of β-cell mass in the GcgNull mice compensated for decreased individual β-cell insulin secretion, which is sufficient to normalize glucose under physiological conditions and conferred some protection after STZ-induced diabetes. NEW & NOTEWORTHY We examined the role of Gcg on β-cell function under normal and high glucose conditions. GcgNull mice had decreased glucose-stimulated insulin secretion, increased β-cell mass, and partial protection against STZ-induced hyperglycemia. Expression of Gcg within the pancreas normalized these endpoints. Intestinal expression of Gcg only normalized β-cell mass and glucose-stimulated insulin secretion. Increased β-cell mass in GcgNull mice likely compensated for decreased insulin secretion normalizing physiological glucose levels and conferring some protection after STZ-induced diabetes [ABSTRACT FROM AUTHOR]

Insulin secretion from β-cells is tightly regulated by local signaling from preproglucagon ( Gcg ) products from neighboring α-cells. Physiological paracrine signaling within the microenvironment of the β-cell is altered after metabolic stress, such as high-fat diet or the β-cell toxin, streptozotocin (STZ). Here, we examined the role and source of Gcg peptides in β-cell function and in response to STZ-induced hyperglycemia. We used whole body Gcg null (Gcg Null ) mice and mice with Gcg expression either specifically within the pancreas (Gcg ΔPanc ) or the intestine (Gcg ΔIntest ). With lower doses of STZ exposure, insulin levels were greater and glucose levels were lower in Gcg Null mice compared with wild-type mice. When Gcg was functional only in the intestine, plasma glucagon-like peptide-1 (GLP-1) levels were fully restored but these mice did not have any additional protection from STZ-induced diabetes. Pancreatic Gcg reactivation normalized the hyperglycemic response to STZ. In animals not treated with STZ, Gcg Null mice had increased pancreas mass via both α- and β-cell hyperplasia and reactivation of Gcg in the intestine normalized β- but not α-cell mass, whereas pancreatic reactivation normalized both β- and α-cell mass. Gcg Null and Gcg ΔIntest mice maintained higher β-cell mass after treatment with STZ compared with control and Gcg ΔPanc mice. Although in vivo insulin response to glucose was normal, global lack of Gcg impaired glucose-stimulated insulin secretion in isolated islets. Congenital replacement of Gcg either in the pancreas or intestine normalized glucose-stimulated insulin secretion. Interestingly, mice that had intestinal Gcg reactivated in adulthood had impaired insulin response to KCl. We surmise that the expansion of β-cell mass in the Gcg Null mice compensated for decreased individual β-cell insulin secretion, which is sufficient to normalize glucose under physiological conditions and conferred some protection after STZ-induced diabetes. NEW & NOTEWORTHY We examined the role of Gcg on β-cell function under normal and high glucose conditions. GcgNull mice had decreased glucose-stimulated insulin secretion, increased β-cell mass, and partial protection against STZ-induced hyperglycemia. Expression of Gcg within the pancreas normalized these endpoints. Intestinal expression of Gcg only normalized β-cell mass and glucose-stimulated insulin secretion. Increased β-cell mass in GcgNull mice likely compensated for decreased insulin secretion normalizing physiological glucose levels and conferring some protection after STZ-induced diabetes.

Nearly 80% of patients that receive bariatric surgery are women, yet mechanistic preclinical studies have focused on males. The goal of this study was to determine the metabolic impact of diet- and surgery-induced weight loss in males, females, and ovariectomized females. All mice were fed a 60% high-fat diet (HFD) before undergoing either vertical sleeve gastrectomy (VSG) or sham surgery. Mice either remained on an HFD or were switched to a standard chow diet postsurgically. When maintained on an HFD, males and females decreased fat mass and improved oral glucose tolerance after VSG. After dietary intervention, additional adiposity was lost in both surgical groups. Ovariectomized females showed a blunted decrease in fat mass on an HFD, but lost significant adiposity after dietary intervention. Energy expenditure was impacted by dietary and not surgical intervention across all groups. Males decreased hepatic triglyceride levels after VSG, which was further decreased after dietary intervention. Intact and ovariectomized females had a blunted decrease in hepatic triglycerides after VSG, but a significant decrease after dietary intervention. The more pronounced effect of VSG on hepatic lipids in males is strongly associated with changes in hepatic expression of genes and microRNAs previously linked to hepatic lipid regulation and systemic energy homeostasis. These data highlight the importance of postsurgical diet on metabolic outcomes across sexes. Furthermore, these data suggest the impact of VSG on hepatic triglycerides is diet-dependent in females and support the hypothesis that males and females achieve similar metabolic outcome, at least within the liver, via distinct mechanisms. NEW & NOTEWORTHY These data highlight the interaction of postsurgical diet after bariatric surgery on metabolic outcomes across sexes. These data suggest the impact of VSG on hepatic triglycerides is diet-dependent in females and support the hypothesis that males and females achieve similar metabolic outcome, at least within the liver, via distinct mechanisms.