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Dr. McLaughlin graduated from Stanford University with honors and distinction in Human Biology, obtained a MS in Public Health at UC Berkeley, and MD at UC San Francisco. She completed her residency in Internal Medicine at Santa Clara Valley Medical Center and her fellowship in Endocrinology, Diabetes, and Metabolism at Stanford University School of Medicine. She is currently a clinician investigator who maintains an active clinic for patients with complicated type 1, type 2, or other forms of diabetes, polycystic ovarian disease, and hypoglcyemia. Her clinical research program includes human studies on obesity, regional fat distribution, and the role of adipocytes and adipose tissue immune cells in promoting insulin resistance and type 2 diabetes. She also conducts studies on the role of incretin hormones in glucose metabolism and postbariatric hypoglycemia, and the use of continuous glucose monitoring and multi-omics methods to define metabolic sub-phenotypes and precision diets for individuals with prediabetes and type 2 diabetes.
Dr. McLaughlin conducts clinical research related to obesity, insulin resistance, diabetes, and cardiovascular disease (CVD). Current studies include: 1) the impact of macronutrient composition on metabolism, DM2 and CVD; 2) comparison of different weight loss diets on metabolism and CVD risk reduction ; 3) role of adipocytes and adipose tissue immune cells in modulating insulin resistance; 4) use of continuous glucose monitoring and multi-omics to define metabolic phenotype and precision diets
Ertugliflozin: Cardioprotective Effects on Epicardial Fat
The purpose of this study is to learn if Sodium-Glucose Cotransporter 2 inhibitor (SGLT2i)
medications enhance beneficial properties of epicardial adipose tissue including metabolic
flexibility, insulin sensitivity, decreased cell size and reduced inflammation.
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Obesity, Weight Loss, and Cardiovascular Disease Risk
The goal of the study is to define the roles played by resistance to insulin-mediated glucose
disposal (insulin resistance) and circulating plasma insulin concentrations in: 1) ability to
lose weight; 2) reduction of risk for coronary heart disease as a result of weight loss. We
hypothesize that in the setting of caloric restriction, manipulating endogenous insulin
concentrations will not alter ability of subjects to lose weight, but will lead to different
reduction in CHD risk factors. To test this hypothesis, two parallel studs will be performed.
First, obese insulin-resistant individuals will be randomized to one of two
equally-hypocaloric diets that vary moderately in proportion of carbohydrate and
mono/polyunsaturated fats (lower carbohydrate diet will be associated with greater reduction
in endogenous insulin secretion). Second, diabetics treated with insulin secretagogues will
be compared to diabetics treated with insulin sensitizers with respect to the same outcomes
(secretagogues increase insulin secretion and insulin sensitizers decrease insulin
concentrations). Endpoints include weight loss, change in insulin resistance, blood pressure,
lipid and lipoproteins, markers of endothelial function, daylong insulin and glucose
concentrations: these will be compared, in each of the parallel studies, between the group
with insulin-stimulating intervention vs the group with the insulin-sparing intervention.
Effect of Liraglutide (Victoza) on Inflammation in Human Adipose Tissue and Blood
The objective of this study is to test the hypothesis that liraglutide (commonly known as
Victoza) can promote an anti-inflammatory macrophage phenotype in human adipose tissue and
blood, thereby reducing localized and systemic inflammation which are risk factors for
cardiovascular disease and may contribute to hyperglycemia. This will be done after 4 weeks
of treatment during which weight will remain stable, and again after 12 weeks, during which
liraglutide-related weight loss occurs.
Stanford is currently not accepting patients for this trial.
For more information, please contact Elizabeth A Colbert, BA, 650-736-2056.
Adipose Tissue Response to Overfeeding in Insulin Resistance-Prone vs. Insulin Sensitive Humans
Obesity has become an epidemic worldwide. Data from our laboratory and others demonstrate
that most of the excess morbidity from obesity is related to insulin resistance (IR). While
total adiposity correlates with insulin resistance, not all obese individuals are IR. When
obese IR individuals lose weight in response to caloric restriction, even moderate loss of
body fat results in improved insulin sensitivity (IS). With massive weight loss, either
dietary or surgical, even the most IR individuals can completely reverse their insulin
resistance. But why is one individual IR at a BMI of 26 and another IS at a BMI of 35? There
must be differences in the manner in which adipose cells/tissue respond to caloric excess and
weight gain. One potentially unifying hypothesis with regard to obesity-associated insulin
resistance is that those individuals who fail to respond to caloric excess/obesity with
adequate adipocyte differentiation and expanded subcutaneous fat storage capacity develop
increased circulating FFAs, ectopic fat deposition, stress on adipocytes, triggering
localized and systemic inflammation and ultimately insulin resistance in skeletal muscle.
Clearly, the best way to examine the human response to obesity is to challenge overweight
individuals with the need to store excess triglyceride in adipose tissue. Specific aims are:
1. Test the hypothesis that impaired adipogenesis and fat storage capacity are associated
with insulin resistance by comparing 1) cell size distribution; 2) gene markers of
adipose cell differentiation; 3) differentiation of isolated preadipocytes in IR-prone
vs IS individuals subjected to caloric excess.
2. Determine if circulating (daylong FFA, two-stage Insulin Suppression Test) and ectopic
fat (MRI liver, CT abdomen) are worsened to a greater degree in IR-prone vs IS
individuals subjected to caloric excess.
3. Determine whether differences in inflammation and/or innate or adaptive immune response
are associated with insulin resistance by comparing differences in resident dendritic
cells, macrophages and their activation profiles, changes in T-cell subpopulations, and
other inflammatory mediators in IR-prone vs IS individuals who are subjected to caloric
excess via overfeeding.
4. Exploratory: Evaluate IR-prone vs IS individuals for evidence of hypoxia and
insufficient angiogenic response in response to caloric excess.