Resume-aware faculty matching

Find professors who actually fit you

Upload your resume. Four AI agents analyze your background, rank the faculty who fit, inspect their recent research, and help you draft outreach — grounded in their actual work, not templates.

Free to startNo credit cardCancel anytime
Top matches Balanced preset
Dr. Sarah Chen
Stanford · Interpretability · NLP
91
Dr. Marcus Holloway
MIT · Robotics · RL
84
Dr. Aisha Okonkwo
CMU · Fairness · HCI
82
Nova · Professor Researcher · re-ranking top 20…
Susan Sam

Susan Sam

· Associate Professor of Medicine

University of Chicago · Endocrinology, Diabetes and Metabolism

Active 1991–2024

h-index23
Citations2.6k
Papers6721 last 5y
Funding$501k
See your match with Susan Sam — sign in to PhdFit.Sign in

About

Susan Sam, MD, MSc, is an adult endocrinologist specializing in the diagnosis and treatment of polycystic ovary syndrome (PCOS). She has clinical interests in reproductive disorders leading to menstrual irregularity in women, type 2 diabetes, and related metabolic disorders. Her research focuses on the metabolic abnormalities associated with PCOS, such as the high risk for developing type 2 diabetes, lipid disorders, and obesity. She examines how abnormalities in fat tissue, including inflammation, contribute to insulin resistance in PCOS. Dr. Sam has received prestigious research grants and has published her findings in scientific journals. She serves as a manuscript reviewer for journals like Clinical Endocrinology, Obesity and Fertility and Sterility, and sits on the editorial board for the Journal of Clinical Endocrinology and Metabolism. Additionally, she is a teacher and mentor to medical students, residents, and endocrinology fellows.

Research topics

  • Endocrinology
  • Medicine
  • Internal medicine

Selected publications

  • Role of multiomics in infertility

    Clinica Chimica Acta · 2024-05-01

    article1st authorCorresponding
  • SAT156 Two Cases Of Hypoglycemia From Inhalation Of Heroin Adulterated With A Sulfonylurea

    Journal of the Endocrine Society · 2023-10-01 · 1 citations

    articleOpen accessSenior author

    Abstract Disclosure: K. Kim: None. J. Hwang: None. S. Sam: None. Context: Hypoglycemic disorders in non-diabetic patients are rare. In the setting of concomitant illicit opioid abuse, hypoglycemia is highly unusual and an underlying cause should be systematically investigated. Objective: We report two separate cases of non-diabetic women both admitted to our intensive care unit for critical hypoglycemia secondary to inhaled heroin containing sulfonylureas. Case 1—A 51 year old female with a history of heroin addiction (on methadone) was brought to the emergency department with altered mental status. She was found to have refractory hypoglycemia and was transferred to the medical intensive care unit (MICU) for monitoring. She reported poor appetite and food intake in the past week and endorsed consuming one alcoholic beverage the night before. Case 2—A 61 year old female with a history of heroin and cocaine abuse was found by the paramedics at home with a decreased level of responsiveness and blood sugar of <30 mg/dL who also required MICU admission. She endorsed using heroin, cocaine and substantial alcohol 2 days prior to admission at a party. She reported 2 episodes of hypoglycemia in the past requiring hospitalization, with no known cause. Kidney and liver disease were ruled out in both subjects. A thorough history including illicit drug use and critical blood samples at the time of hypoglycemia including drug toxicity screen, sulfonylurea screen were obtained. Labs demonstrated an insulin-mediated hypoglycemia and positive sulfonylurea screen for glipizide in both patients. Results: Because of their non-diabetic status, their compelling history and the results of their comprehensive laboratory work-up, we conclude that these subjects had a common exposure- insufflation of heroin contaminated with an oral hypoglycemic agent shortly before their admissions with critical hypoglycemia and clinical instability. Conclusions: This is the first report of hypoglycemia related to inhalation of heroin adulterated with the sulfonylurea glipizide. Frequently heroin is intentionally mixed with other agents (diphenhydramine) to increase the volume for sale, optimize the drug uptake or to ease the side effects. These cases highlight the importance of obtaining a thorough clinical history including potential illicit drug use, acquiring timely and appropriate laboratory samples for toxicologic analysis, and interpreting the findings to curb a potentially deadly epidemic. Presentation: Saturday, June 17, 2023

  • THU611 Circadian Misalignment Of Melatonin Secretion In Adrenal Insufficiency (AI)

    Journal of the Endocrine Society · 2023-10-01 · 1 citations

    articleOpen access

    Abstract Disclosure: M. Darji: None. S. Pannain: None. S. Sam: None. E. Van Cauter: None. E.C. Hanlon: None. Background: Despite glucocorticoid replacement, the mortality risk of AI remains markedly elevated. Under normal conditions, the circadian rhythm of endogenous cortisol levels is a major internal synchronizing signal between central and peripheral circadian clocks. There is increasing evidence indicating that circadian misalignment has a host of adverse effects, including increased cardio-metabolic risk. The present study aimed to assess circadian function in AI patients, as compared to individually-matched healthy subjects, under controlled laboratory conditions. The 24-h profile of melatonin, normally secreted exclusively at night, was used as the marker of central circadian timing. The 24-h profile of leptin was used as a marker of peripheral circadian function. Methods: Plasma cortisol, melatonin, and leptin were measured over a 24-h period every 30-60 minutes under controlled light-dark, sleep-wake and dietary conditions. A best-fit curve was calculated for each individual hormonal profile using a locally weighted nonlinear regression procedure with a window of 4 hours. The peak and the nadir were defined as the maximum and minimum of the best-fit curve, respectively. The amplitude was defined as half of the difference between the peak and the nadir. Sleep was polygraphically recorded. During daytime hours, the participants completed validated questionnaires assessing Vigor, Mood and Sleepiness. Results: Complete data sets were obtained in 15 AI patients (12 women; age: 47.9 ±12.5 years, BMI: 26.6 ± 12.5 kg/m2; mean ± SD). Twelve AI patients were on hydrocortisone treatment (total dose range: 20 to 40mg/day, number of doses: 1-5 /day) and 3 were on prednisone treatment. Controls (n=15, 12 women) were aged 48.5 ±14.5 years with BMI of 26.5 ± 5.4 kg/m2. The amplitude of the cortisol profile was wider in AI patients, relative to controls, with a higher morning peak and an extended and lower nocturnal nadir. Unexpectedly, we observed a marked difference in the melatonin profile in AI patients as compared to controls. A daytime phase of elevated melatonin levels, culminating prior to lights off while the patients were awake, was detected in 9 of the 15 AI patients. The nocturnal elevation persisted with a similar amplitude to that observed in controls but was advanced by 1-2 hours. The 24-h leptin profile was similar in the two groups. The presence of a daytime melatonin peak in AI patients was associated with lower ratings of vigor and mood, and higher ratings of sleepiness. Conclusion: Glucocorticoid treatment to replace the endogenous levels and circadian rhythmicity of cortisol in AI may impact central circadian timing, resulting in daytime, in addition to nighttime, release of melatonin. This finding suggests that exogenous cortisol replacement that does not mimic a normal 24-h rhythm, may cause central circadian dysfunction and contribute to alterations in mood, vigor and sleepiness. Presentation: Thursday, June 15, 2023

  • Polycystic Ovary Syndrome

    2022-01-28

    book-chapterSenior author

    Abstract Insulin resistance is common among women with PCOS independent of adiposity. However, the severity of insulin resistance in these women worsens with obesity especially in those who present with the classical phenotype of PCOS (NIH criteria) consisting of hyperandrogenism and menstrual irregularity. Hence, obese women with PCOS, especially those with the classic phenotype of PCOS, are at high risk for metabolic complications. These complications include type 2 diabetes (DM2), metabolic syndrome, dyslipidaemia and obstructive sleep apnoea (OSA). Additionally, these women are at increased risk for cardiovascular disease even though the exact risk for this complication is not established. Due to heightened risk for metabolic disorders, close screening and follow-up for development of glucose intolerance, metabolic syndrome, and OSA is essential and is supported by current guidelines. Management of women with PCOS is individualized and should depend on the patient’s symptoms as well as their risk for development of various complications.

  • Weight loss and β‐cell responses following gastric banding or pharmacotherapy in adults with impaired glucose tolerance or type 2 diabetes: a randomized trial

    Obesity · 2022-07-27

    articleOpen access

    OBJECTIVE: The extent to which weight loss contributes to increases in insulin sensitivity (IS) and β-cell function after surgical or medical intervention has not been directly compared in individuals with impaired glucose tolerance or newly diagnosed type 2 diabetes. METHODS: The Restoring Insulin Secretion (RISE) Study included adults in the Beta-Cell Restoration Through Fat Mitigation Study (n = 88 randomized to laparoscopic gastric banding or metformin [MET]) and the Adult Medication Study (n = 267 randomized to placebo, MET, insulin glargine/MET, or liraglutide + MET [L + M]). IS and β-cell responses were measured at baseline and after 12 months by modeling of oral glucose tolerance tests and during arginine-stimulated hyperglycemic clamps. Linear regression models assessed differences between and within treatments over time. RESULTS: BMI decreased in all treatment groups, except placebo, at 12 months. IS increased in all arms except placebo and was inversely correlated with changes in BMI. L + M was the only treatment arm that enhanced multiple measures of β-cell function independent of weight loss. Insulin secretion decreased in the laparoscopic gastric banding arm proportional to increases in IS, with no net benefit on β-cell function. CONCLUSIONS: Reducing demand on the β-cell by improving IS through weight loss does not reverse β-cell dysfunction. L + M was the only treatment that enhanced β-cell function.

  • Baseline Predictors of Glycemic Worsening in Youth and Adults With Impaired Glucose Tolerance or Recently Diagnosed Type 2 Diabetes in the Restoring Insulin Secretion (RISE) Study

    Diabetes Care · 2021 · 44 citations

    1st authorCorresponding
    • Medicine
    • Internal medicine
    • Endocrinology

    OBJECTIVE: To identify predictors of glycemic worsening among youth and adults with impaired glucose tolerance (IGT) or recently diagnosed type 2 diabetes in the Restoring Insulin Secretion (RISE) Study. RESEARCH DESIGN AND METHODS: increase ≥0.5% from baseline). RESULTS: < 0.05). CONCLUSIONS: Glycemic worsening was more common among youth than adults with IGT or recently diagnosed type 2 diabetes, predicted by lower baseline β-cell responses in both groups, hyperglycemia in youth, and insulin resistance in adults.

  • Effect of Medical and Surgical Interventions on α-Cell Function in Dysglycemic Youth and Adults in the RISE Study

    Diabetes Care · 2021-06-16 · 5 citations

    articleOpen access

    OBJECTIVE To compare effects of medications and laparoscopic gastric band surgery (LB) on α-cell function in dysglycemic youth and adults in the Restoring Insulin Secretion (RISE) Study protocols. RESEARCH DESIGN AND METHODS Glucagon was measured in three randomized, parallel, clinical studies: 1) 91 youth studied at baseline, after 12 months on metformin alone (MET) or glargine followed by metformin (G/M), and 3 months after treatment withdrawal; 2) 267 adults studied at the same time points and treated with MET, G/M, or liraglutide plus metformin (L+M) or given placebo (PLAC); and 3) 88 adults studied at baseline and after 12 and 24 months of LB or MET. Fasting glucagon, glucagon suppression by glucose, and acute glucagon response (AGR) to arginine were assessed during hyperglycemic clamps. Glucagon suppression was also measured during oral glucose tolerance tests (OGTTs). RESULTS No change in fasting glucagon, steady-state glucagon, or AGR was seen at 12 months following treatment with MET or G/M (in youth and adults) or PLAC (in adults). In contrast, L+M reduced these measures at 12 months (all P ≤ 0.005), which was maintained 3 months after treatment withdrawal (all P &amp;lt; 0.01). LB in adults also reduced fasting glucagon, steady-state glucagon, and AGR at 12 and 24 months (P &amp;lt; 0.05 for all, except AGR at 12 months [P = 0.098]). Similarly, glucagon suppression during OGTTs was greater with L+M and LB. Linear models demonstrated that treatment effects on glucagon with L+M and LB were largely associated with weight loss. CONCLUSIONS Glucagon concentrations were reduced by L+M and LB in adults with dysglycemia, an effect principally attributable to weight loss in both interventions.

  • Obstructive Sleep Apnea, Glucose Tolerance, and β-Cell Function in Adults With Prediabetes or Untreated Type 2 Diabetes in the Restoring Insulin Secretion (RISE) Study

    Diabetes Care · 2021-02-05 · 26 citations

    articleOpen access

    OBJECTIVE Obstructive sleep apnea (OSA) is associated with insulin resistance and has been described as a risk factor for type 2 diabetes. Whether OSA adversely impacts pancreatic islet β-cell function remains unclear. We aimed to investigate the association of OSA and short sleep duration with β-cell function in overweight/obese adults with prediabetes or recently diagnosed, treatment-naive type 2 diabetes. RESEARCH DESIGN AND METHODS Two hundred twenty-one adults (57.5% men, age 54.5 ± 8.7 years, BMI 35.1 ± 5.5 kg/m2) completed 1 week of wrist actigraphy and 1 night of polysomnography before undergoing a 3-h oral glucose tolerance test (OGTT) and a two-step hyperglycemic clamp. Associations of measures of OSA and actigraphy-derived sleep duration with HbA1c, OGTT-derived outcomes, and clamp-derived outcomes were evaluated with adjusted regression models. RESULTS Mean ± SD objective sleep duration by actigraphy was 6.6 ± 1.0 h/night. OSA, defined as an apnea-hypopnea index (AHI) of five or more events per hour, was present in 89% of the participants (20% mild, 28% moderate, 41% severe). Higher AHI was associated with higher HbA1c (P = 0.007). However, OSA severity, measured either by AHI as a continuous variable or by categories of OSA severity, and sleep duration (continuous or &amp;lt;6 vs. ≥6 h) were not associated with fasting glucose, 2-h glucose, insulin sensitivity, or β-cell responses. CONCLUSIONS In this baseline cross-sectional analysis of the RISE clinical trial of adults with prediabetes or recently diagnosed, untreated type 2 diabetes, the prevalence of OSA was high. Although some measures of OSA severity were associated with HbA1c, OSA severity and sleep duration were not associated with measures of insulin sensitivity or β-cell responses.

  • Obstructive Sleep Apnea, Glucose Tolerance, and β-Cell Function in Adults With Prediabetes or Untreated Type 2 Diabetes in the Restoring Insulin Secretion (RISE) Study

    2021-02-19 · 1 citations

    preprintOpen access

    &lt;b&gt;Objective:&lt;/b&gt; Obstructive sleep apnea (OSA) is associated with insulin resistance and has been described as a risk factor for type 2 diabetes. Whether OSA adversely impacts pancreatic islet beta-cell function remains unclear. We aimed to investigate the association of OSA and short sleep duration with beta-cell function in overweight/obese adults with prediabetes or recently-diagnosed, treatment-naïve type 2 diabetes. &lt;p&gt;&lt;b&gt;Research Design and Methods:&lt;/b&gt; 221 adults (57.5% men, age 54.5±8.7 years, BMI 35.1±5.5 kg/m&lt;sup&gt;2&lt;/sup&gt;) completed one week of wrist actigraphy and one night of polysomnography before undergoing a 3-h oral glucose tolerance test (OGTT) and a two-step hyperglycemic clamp. Associations of measures of OSA and actigraphy-derived sleep duration with HbA1c, OGTT-derived and clamp-derived outcomes were evaluated with adjusted regression models.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Results:&lt;/b&gt; Mean±SD objective sleep duration by actigraphy was 6.6±1.0 hours/night. OSA defined as an apnea-hypopnea index (AHI) ≥5 events per hour was present in 89% of the participants; 20% mild, 28% moderate and 41% severe. Higher AHI was associated with higher HbA1c (p =0.007). However, OSA severity, measured by either AHI as a continuous variable or by categories of OSA severity, and sleep duration (continuous or &lt;6 h vs. ≥6 h) were not associated with fasting glucose, 2-h glucose, insulin sensitivity or beta-cell responses.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Conclusion:&lt;/b&gt; In this baseline cross-sectional analysis of the RISE clinical trial of adults with prediabetes or recently-diagnosed, untreated type 2 diabetes, the prevalence of OSA was high. Although some measures of OSA severity were associated with HbA1c, OSA severity and sleep duration were not associated with measures of insulin sensitivity or beta-cell responses.&lt;/p&gt;

  • Obstructive Sleep Apnea, Glucose Tolerance, and β-Cell Function in Adults With Prediabetes or Untreated Type 2 Diabetes in the Restoring Insulin Secretion (RISE) Study

    2021-02-19

    preprintOpen access

    &lt;b&gt;Objective:&lt;/b&gt; Obstructive sleep apnea (OSA) is associated with insulin resistance and has been described as a risk factor for type 2 diabetes. Whether OSA adversely impacts pancreatic islet beta-cell function remains unclear. We aimed to investigate the association of OSA and short sleep duration with beta-cell function in overweight/obese adults with prediabetes or recently-diagnosed, treatment-naïve type 2 diabetes. &lt;p&gt;&lt;b&gt;Research Design and Methods:&lt;/b&gt; 221 adults (57.5% men, age 54.5±8.7 years, BMI 35.1±5.5 kg/m&lt;sup&gt;2&lt;/sup&gt;) completed one week of wrist actigraphy and one night of polysomnography before undergoing a 3-h oral glucose tolerance test (OGTT) and a two-step hyperglycemic clamp. Associations of measures of OSA and actigraphy-derived sleep duration with HbA1c, OGTT-derived and clamp-derived outcomes were evaluated with adjusted regression models.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Results:&lt;/b&gt; Mean±SD objective sleep duration by actigraphy was 6.6±1.0 hours/night. OSA defined as an apnea-hypopnea index (AHI) ≥5 events per hour was present in 89% of the participants; 20% mild, 28% moderate and 41% severe. Higher AHI was associated with higher HbA1c (p =0.007). However, OSA severity, measured by either AHI as a continuous variable or by categories of OSA severity, and sleep duration (continuous or &lt;6 h vs. ≥6 h) were not associated with fasting glucose, 2-h glucose, insulin sensitivity or beta-cell responses.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Conclusion:&lt;/b&gt; In this baseline cross-sectional analysis of the RISE clinical trial of adults with prediabetes or recently-diagnosed, untreated type 2 diabetes, the prevalence of OSA was high. Although some measures of OSA severity were associated with HbA1c, OSA severity and sleep duration were not associated with measures of insulin sensitivity or beta-cell responses.&lt;/p&gt;

Recent grants

Frequent coauthors

  • Kristen J. Nadeau

    University of Colorado Anschutz Medical Campus

    66 shared
  • Kieren J. Mather

    52 shared
  • Steven E. Kahn

    University of Washington

    46 shared
  • Kristina M. Utzschneider

    University of Puget Sound

    42 shared
  • Babak Mokhlesi

    Rush University

    40 shared
  • Sharon L. Edelstein

    George Washington University

    39 shared
  • Elena Barengolts

    Jesse Brown VA Medical Center

    36 shared
  • Silva Arslanian

    34 shared
  • Resume-aware match score
  • Save to shortlist
  • AI-drafted outreach

See your match with Susan Sam

PhdFit ranks faculty by your research interests, methods, and publications — grounded in their actual work, not templates.

  • Free to start
  • No credit card
  • 30-second signup