About

The provided page text does not contain a professional biography or specific research information about Professor Anika K. Anam. Therefore, there is no available biographical content to summarize.

Research topics

• Medicine
• Internal medicine
• Endocrinology
• Biochemistry
• Physical therapy
• Biology
• Intensive care medicine

Selected publications

• Implementing an Innovative Transgender and Gender Diverse Health Curriculum for Physician Assistant (PA) Students

  AACE Endocrinology and Diabetes · 2025-10-15

  articleOpen access1st authorCorresponding

  Background: The large gaps in gender diverse medical knowledge among clinicians contribute to the healthcare disparities experienced by transgender and gender diverse (TGD) individuals.Though many physician assistant (PA) programs provide TGD content, most of this content is focused on medical interviewing. Barriers to teaching TGD health topics include low faculty knowledge and lack of time. We created a video-based TGD curriculum to increase PA student medical knowledge and confidence in gender-affirming hormone therapy management. Methods: Our 90-minute, novel curriculum targeting PA students was based on a video case with a transgender woman presenting for gender-affirming therapy. We employed learning strategies including didactics, active learning, and video. Medical knowledge and attitudes towards TGD individuals before and after the intervention were measured using t tests. Results: > .05). Conclusions: This workshop taught PA students how to prescribe and monitor gender-affirming hormone therapy and provide basic counseling by combining multiple learning techniques. By significantly increasing students' self-perception of confidence and medical knowledge in TGD care, and altering attitudes towards TGD individuals, our workshop is effective by increasing preparedness for students to engage in TGD care. This workshop can be easily adapted for myriad healthcare trainees.

  PublisherOA PDFDOI

• Newer Glucose-Lowering Medications and Potential Role in Metabolic Management of PCOS

  Springer eBooks · 2022 · 2 citations

  1st authorCorresponding
  • Medicine
  • Intensive care medicine
  PublisherDOI

• Insulin increases placental triglyceride as a potential mechanism for fetal adiposity in maternal obesity

  Molecular Metabolism · 2022 · 18 citations

  1st authorCorresponding
  • Endocrinology
  • Internal medicine
  • Biology

  OBJECTIVE: Maternal obesity increases the incidence of excess adiposity in newborns, resulting in lifelong diabetes risk. Elevated intrauterine fetal adiposity has been attributed to maternal hyperglycemia; however, this hypothesis does not account for the increased adiposity seen in newborns of mothers with obesity who have euglycemia. We aimed to explore the placental response to maternal hyperinsulinemia and the effect of insulin-like growth factor 2 (IGF-2) in promoting fetal adiposity by increasing storage and availability of nutrients to the fetus. METHODS: We used placental villous explants and isolated trophoblasts from normal weight and obese women to assess the effect of insulin and IGF-2 on triglyceride content and insulin receptor signaling. Stable isotope tracer methods were used ex vivo to determine effect of hormone treatment on de novo lipogenesis (DNL), fatty acid uptake, fatty acid oxidation, and esterification in the placenta. RESULTS: Here we show that placentae from euglycemic women with normal weight and obesity both have abundant insulin receptor. Placental depth and triglyceride were greater in women with obesity compared with normal weight women. In syncytialized placental trophoblasts and villous explants, insulin and IGF-2 activate insulin receptor, induce expression of lipogenic transcription factor SREBP-1 (sterol regulatory element-binding protein 1), and stimulate triglyceride accumulation. We demonstrate elevated triglyceride is attributable to increased esterification of fatty acids, without contribution from DNL and without an acceleration of fatty acid uptake. CONCLUSIONS: Our work reveals that obesity-driven aberrations in maternal metabolism, such as hyperinsulinemia, alter placental metabolism in euglycemic conditions, and may explain the higher prevalence of excess adiposity in the newborns of obese women.

  PublisherDOI

• Update on Osteoporosis Screening and Management

  Medical Clinics of North America · 2021 · 227 citations

  1st authorCorresponding
  • Medicine
  • Internal medicine
  • Physical therapy
  PublisherDOI

• Comment on Rhee et al. Association Between Glycemic Status and the Risk of Parkinson Disease: A Nationwide Population-Based Study. Diabetes Care 2020;43:2169–2175

  Diabetes Care · 2020-05-10 · 1 citations

  letterOpen accessSenior author

  Metabolic diseases, such as diabetes and obesity, increase susceptibility for additional long-term complications, including Parkinson disease (PD). Rhee et al. (1) aim to address this issue by using a large data set obtained from the Korean National Health Insurance consisting of a sample of over 15 million individuals aged 40 years and older who had undergone routine checkups between 2009 and 2010. They evaluated diabetes as a risk factor for PD by analyzing how PD risk varies according to baseline glucose tolerance status, diabetes duration, and comorbidities such as obesity, cardiovascular disease, and cerebrovascular disease. The authors demonstrate that the risk of PD is increased in patients with diabetes and that the incidence of PD is proportional to the degree of exposure to hyperglycemia. The finding that the diagnosis of diabetes itself is not enough …

  PublisherOA PDFDOI

• OR20-07 Placentas from Obese Women Are Resistant to the Effect of Insulin on Triglyceride Content Ex Vivo

  Journal of the Endocrine Society · 2020-04-01

  articleOpen access1st authorCorresponding

  Abstract Background: Obesity affects 25% of pregnant women and is associated with a higher risk of neonatal complications, such as macrosomia and increased adiposity. The placenta may contribute to neonatal adiposity by accumulating and transferring excess lipid in response to maternal hyperinsulinemia. We previously found that insulin promotes a 3-fold increase in placental triglyceride (TG) content in lean women. We hypothesized that obese women have higher placental insulin resistance compared to lean women[FC1] with respect to TG content. Methods: Healthy, lean women (n=12; mean age 34±1 yrs; BMI 22±0.4 kg/m2) and non-diabetic, obese women (n=9; mean age 32±2 yrs; BMI 33±0.4 kg/m2, p<0.0001) consented for placenta collection at elective c-section under fasting conditions. Placental villous explants were immediately flash frozen or cultured for 24 hours, starved, then treated for 48 hours with 0.1nM, 1nM, 10nM, or 100nM of insulin, or vehicle. Lipids were extracted from basal and treated explants using a chloroform-methanol separation protocol. TG content was quantified by spectrophotometer and normalized to weight. Data were analyzed by two-way ANOVA. Results: Basal placenta tissue from obese women contained a 1.5-fold higher level of TG compared to lean women (9.4±0.5 vs 5.7±0.5 mcg/mg, p=0.001). Placental response to insulin in lean women peaked at 1nM insulin (20.2±3.3 mcg/mg), and plateaued at higher doses of 10nM (18.6±3.3 mcg/mg) and 100nM (22.8±2.8 mcg/mg, p=NS respectively). In contrast, placenta explants from obese women required the highest insulin dose of 100 nM for maximal response (23.6±3.2 mcg/mg), and showed a gradual dose response from 0.1 nM insulin (9.5±2), 1nM (14.8±2), 10 nM (16.9±3). At 100nM insulin, the difference in TG content was variable, but on average was 2-fold higher than vehicle treated placenta (vs 11.8±2.5[FC2] [AA3] mcg/mg, p=0.002). Conclusion: Our findings indicate that placenta from obese women develop insulin resistance similar to peripheral tissues, which can be overcome by high insulin doses. This placental insulin resistance likely occurs in response to chronic hyperinsulinemia, leading to interference of insulin signaling pathways, and may protect the neonate from excessive nutrient flux.

  PublisherDOI

• SAT-LB041 Insulin and IGF-2 Equally Regulate Placental Triglyceride Content

  Journal of the Endocrine Society · 2019-04-01

  articleOpen access1st authorCorresponding

  Background: Obesity affects 25% of pregnant women and is associated with a higher risk of neonatal complications, such as macrosomia and increased adiposity. In addition to transporting maternal nutrients to the fetus, the placenta receives maternal hormone signals and synthesizes paracrine hormones which influence nutrient flux to the fetus. Obese women were shown to have higher placental lipid content compared to lean women, but the regulation of placental lipid metabolism is unknown. We hypothesized that insulin regulates lipid metabolism in the placenta by activating IR-B, which is the insulin receptor (IR) isoform characterized as having metabolic activity. Methods: Healthy, lean women (n=7) of mean age 34.4 ± 1.4 years and BMI 21.5 ± 0.5 kg/m2 consented for placental collection at elective c-section. Full thickness placental samples from multiple quadrants were obtained. Villous explants were cultured for 24 hours. After 4-hour starvation, explants were treated for 48 hours with insulin 100nM, IGF-1 100nM, IGF-2 100nM, or vehicle. Lipids were extracted from homogenized explants using a chloroform-methanol separation protocol. Triglyceride (TG) content was quantified by colorimetric spectrophotometer and normalized to explant weight. Data were analyzed by one-way ANOVA with a Tukey’s multiple comparisons test. Results: In placenta explants from lean women, insulin induced a 2.5-fold increase in triglyceride content, relative to vehicle (19.8 ± 3 vs 7.3 ± 1.5 mcg/mg, p= 0.002). Similarly, IGF-2 promoted a 3.4-fold increase compared to vehicle-treated placental tissue (24.9 ± 3.3 mcg/mg, p= 0.0002). In contrast, IGF-1 did not significantly alter TG levels (12.7 ± 2.9 vs 10.2 ± 2.6 mcg/mg, p= NS). Conclusions: We show that placental triglyceride content is equally regulated by maternal insulin and placenta-synthesized IGF-2. Since IGF-2 has a high affinity for IR-A and minimal affinity for IR-B, these data indicate that IR-A likely plays a key role in placental lipid metabolism. These findings are novel since IR-A activity is generally characterized as mitogenic, rather than metabolic. Notably, IGF-1, which activates IGF-1R, does not play a role in placental lipid metabolism in vitro. Hyperinsulinemia due to maternal obesity may alter placental triglyceride storage and thus promote neonatal adiposity through greater availability, independent of circulating maternal triglyceride levels. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. Abstracts presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.

  PublisherDOI

• The Selective Progesterone Receptor Modulator Ulipristal Acetate Inhibits the Activity of the Glucocorticoid Receptor

  The Journal of Clinical Endocrinology & Metabolism · 2019-10-29 · 16 citations

  articleOpen access

  CONTEXT: The selective progesterone modulator ulipristal acetate (ulipristal) offers a much-needed therapeutic option for the clinical management of uterine fibroids. Although ulipristal initially passed safety evaluations in Europe, postmarketing analysis identified cases of hepatic injury and failure, leading to restrictions on the long-term use of ulipristal. One of the factors potentially contributing to significant side effects with the selective progesterone modulators is cross-reactivity with other steroid receptors. OBJECTIVE: To determine whether ulipristal can alter the activity of the endogenous glucocorticoid receptor (GR) in relevant cell types. DESIGN: Immortalized human uterine fibroid cells (UtLM) and hepatocytes (HepG2) were treated with the synthetic glucocorticoid dexamethasone and/or ulipristal. Primary uterine fibroid tissue was isolated from patients undergoing elective gynecological surgery and treated ex vivo with dexamethasone and/or ulipristal. In vivo ulipristal exposure was performed in C57Bl/6 mice to measure the effect on basal gene expression in target tissues throughout the body. RESULTS: Dexamethasone induced the expression of established glucocorticoid-target genes period 1 (PER1), FK506 binding protein 51 (FKBP5), and glucocorticoid-induced leucine zipper (GILZ) in UtLM and HepG2 cells, whereas cotreatment with ulipristal blocked the transcriptional response to glucocorticoids in a dose-dependent manner. Ulipristal inhibited glucocorticoid-mediated phosphorylation, nuclear translocation, and DNA interactions of GR. Glucocorticoid stimulation of PER1, FKBP5, and GILZ was abolished by cotreatment with ulipristal in primary uterine fibroid tissue. The expression of glucocorticoid-responsive genes was decreased in the lung, liver, and uterus of mice exposed to 2 mg/kg ulipristal. Interestingly, transcript levels of Fkbp5 and Gilz were increased in the hippocampus and pituitary. CONCLUSIONS: These studies demonstrate that ulipristal inhibits endogenous glucocorticoid signaling in human fibroid and liver cells, which is an important consideration for its use as a long-term therapeutic agent.

  PublisherOA PDFDOI

• Postmenopausal Women with Endometrial Cancer Have Greater Metabolic Dysfunction and Higher BMI than Women with Benign Endometrium

  Diabetes · 2018-06-22

  article

  Obesity is an independent risk factor for endometrial adenocarcinoma (EC), yet it is unknown which attributes of obesity contribute to EC pathogenesis. We hypothesize that heterogeneity in metabolic health distinguishes which obese women are at risk for EC. We previously found that more premenopausal women with pre-malignant hyperplasia had type 2 diabetes and dyslipidemia than women with benign hyperplasia (BH), despite similar BMI. BH is the ideal control condition since presenting symptoms are similar, yet malignant transformation is negligible. Thus, we sought to compare metabolic abnormalities in postmenopausal women with EC and BH. We reviewed medical records of 284 women who received a biopsy/hysterectomy at our center over 3 years. We examined non-Hispanic white women age 50-65 years with BMI 25-50 kg/m2, to limit variability in factors known to affect metabolism. 122 women had histologically confirmed EC (n=74) or BH (n=48), and 60% had lab data. Variables were analyzed by chi-squared or Student’s T test. Women with EC were older (58 ± 0.5 vs. 53 ± 0.4 years, p<0.0001) and had higher BMI (37 ± 1 vs. 32 ± 1 kg/m2, p<0.0001) than women with BH. BMI distribution was markedly different between groups, with a higher frequency and greater severity of obesity among women with EC (p<0.0001). More women with EC than BH had type 2 diabetes (19% vs. 4%, p<0.05) and hypertension (54% vs. 25%, p<0.01). Women with EC had higher triglycerides (140 ± 12 vs. 110 ± 13 mg/dL, p<0.05) and lower HDL (55 ± 2 vs. 60 ± 4 mg/dL, p=NS). However, these differences can be explained by the skewed BMI distribution. LDL and total cholesterol as well as statin use (20% vs. 25%) were similar between groups (p=NS). The striking differences in BMI among postmenopausal women with EC and BH highlights the role of obesity in EC pathogenesis. Since BMI affects metabolism, a prospective study of BMI-matched women is necessary to determine whether metabolic dysregulation independently influences cancer development. Disclosure K.M. Cooke: None. E. Dun: None. A.K. Anam: None. C. Flannery: None.

  PublisherDOI

• Benefit of Albumin Infusion in Hospitalized Patients With Cirrhosis and Hyponatremia:A Retrospective Cohort Study

  Journal of Gastroenterology and Hepatology Research · 2017-01-01 · 8 citations

  articleOpen access

  AIM: To investigate the optimal intravenous fluid for resuscitation of hospitalized patients with cirrhosis and hyponatremia and analyze their outcomes. MATERIALS AND METHODS: In this retrospective cohort study, consecutive patients with hyponatremia and cirrhosis, portal hypertension, ascites, or hepatic encephalopathy receiving resuscitative fluids and hospitalized between 1/2011 and 12/2014 were analyzed. Patient characteristics, quantity and type of fluid administered, change in serum sodium, and 6-month mortality were recorded. RESULTS: A total of 146 eligible patients were identified, of which 62% (91/146) received primarily crystalloid and 38% (55/146) primarily albumin resuscitative fluid. Those within the albumin cohort were more likely to receive diuretics (82% vs 56%, p = 0.001), have a history of refractory ascites (56% vs 21%, p < 0.001), ascites on admission (96% vs 60%, p < 0.001), higher admission body mass (81.6 kg vs 75.5 kg, p = 0.04), higher creatinine (152.9 µmol/L vs 130.8 µmol/L, p = 0.03), and higher model for end-stage liver disease (MELD) score (23.0 vs 18.9, p = 0.002) compared to those in the crystalloid cohort. Fluid selection did not impact sodium correction (p = 0.67). In multivariate analysis, receiving albumin and having higher baseline serum albumin were both associated with reduced 6-month mortality, odds ratio of 0.06 (p = 0.013) and 0.13 (p = 0.035), respectively. CONCLUSIONS: Fluid selection in patients with cirrhosis and hyponatremia insignificantly impacted sodium correction. Albumin infusion was associated with reduced 6-month mortality. Larger prospective trials are required to investigate this relationship.

  PublisherOA PDFDOI

Frequent coauthors

• Arun Jesudian

  Cornell University

  37 shared

• Monica Saumoy

  32 shared

• David Wan

  Presbyterian Hospital

  32 shared

• Nicole Shen

  16 shared

• Brian P. Bosworth

  16 shared

• Kunal Karia

  Kaiser Permanente San Francisco Medical Center

  16 shared

• Yecheskel Schneider

  St. Luke's University Health Network

  5 shared

• Clare A. Flannery

  Agilent Technologies (Germany)

  5 shared

Labs

• Endocrinology & MetabolismPI

Awards & honors

• Travel Award - Early Career Forum (2018)
• Future Leaders Advancing Research in Endocrinology (FLARE) (…
• Rubin Certificate of Commendation (2013)
• Harold A. Lyons, MD Award for Excellence in Clinical Medicin…
• Alpha Omega Alpha Honor Medical Society (2012)