UC Berkeley

Graduate Student Instructor

Human Endocrinology, Fall 2013. Responsibilities will include preparing weekly review sessions for class material and journal review; preparing and grading exams for 160 students, and hold weekly office hours.

UC Berkeley

Graduate Student Instructor

Hormones and Behavior, Spring 2013. Responsibilities included learning and teaching students material from class lecture in three smaller sections of 20 to 25 students each (total of about 70 students). Critiqued student group presentations, reviewing, preparing, proctoring and grading of exams; held weekly office hours.

UC Berkeley

Reviewer for the Biology Fellows Program Grant, which provides disadvantaged UC Berkeley undergraduates a stipend to support their efforts in research and development. The purpose of this grant is to support diversity. minority outreach in the sciences, and financial support to deserving students.

Stanford University School of Medicine

Postdoctoral Resarch Fellow

Serving in a dual-capacity as Research fellow and Research coordinator for multiple projects within our lab group:

Primary clinical trials: Applying the use of deuterated water (2H2O) in overweight insulin sensitive and insulin resistant humans, we are investigating the effects of weight-gain on adipocyte function to determine if adipocyte dysfunction leads to the onset of insulin resistance.

Secondary clinical trials: In a large collaborative study with Dr. Michael Snyder, we examined the microbiome in prediabetic and healthy lean and overweight humans to investigate how changes in an individual's microbiome may determine metabolic profile changes, with an emphasis of one’s risk for the development of type 2 diabetes progresses over time. This study is currently on-going.

Tertiary clinical trial: Investigating post-bariatric surgery complications.

University of California, Davis

Postdoctoral Scholar

As co-investigator on our clinical trials exploring the mechanisms of cardiovascular disease and type 2 diabetes disease risk following consumption of dietary sugar, I assisted in various aspects of our study protocol including assisting in the conduct of inpatient metabolic testing (i.e. conducting hyperinsulinemic euglycemic clamp), processing of human specimen for lipid quantification, metabolic profiling, preparation of manuscripts, conference presentations, and subject recruitment and screening.

My collaborations with scientists at UC Davis and other institutions within the State of California have introduced new approaches and advanced technologies that will produce novel findings to aid in our exploration of mechanisms of metabolic disease risk.

University of California, Davis

Assistant Adjunct Professor

My research focuses on understanding the genetic and molecular mechanisms through which added sugar consumption and psychological stress affects cardiometabolic health risks in African-American women.

University of California, San Francisco

Visiting Research Scholar

I initiated a collaboration with the University of California, San Francisco, Institute for Human Genetics to conduct a pilot study investigating potential miRNA biomarkers of insulin resistance in humans consuming sugar-sweetened beverages. Findings may have implications for epigenetic effects of dietary added sugar and risk for metabolic disease.

In vivo 2H2O administration reveals impaired triglyceride storage in adipose tissue of insulin-resistant humans.

Journal of Lipid Research

Indirect evidence suggests that impaired triglyceride storage in the subcutaneous fat depot contributes to the development of insulin resistance via lipotoxicity. We directly tested this hypothesis by measuring, in vivo, triglyceride (TG) synthesis, de novo lipogenesis (DNL), adipocyte proliferation, and insulin-suppression of lipolysis in subcutaneous adipose tissue of BMI-matched individuals classified as insulin resistant (IR) or sensitive (IS). These results provide direct, in vivo evidence for impaired TG storage in subcutaneous adipose tissue of IR as compared with IS. Relative inability to store TG in the subcutaneous depot may represent a mechanism contributing to the development of insulin resistance in the setting of obesity.

In vivo 2H2O administration reveals impaired triglyceride storage in adipose tissue of insulin-resistant humans.

Journal of Lipid Research

Indirect evidence suggests that impaired triglyceride storage in the subcutaneous fat depot contributes to the development of insulin resistance via lipotoxicity. We directly tested this hypothesis by measuring, in vivo, triglyceride (TG) synthesis, de novo lipogenesis (DNL), adipocyte proliferation, and insulin-suppression of lipolysis in subcutaneous adipose tissue of BMI-matched individuals classified as insulin resistant (IR) or sensitive (IS). These results provide direct, in vivo evidence for impaired TG storage in subcutaneous adipose tissue of IR as compared with IS. Relative inability to store TG in the subcutaneous depot may represent a mechanism contributing to the development of insulin resistance in the setting of obesity.

Metabolic markers, regional adiposity, and adipose cell size: relationship to insulin resistance in African-American as compared with Caucasian women.

International Journal of Obesity

In vivo 2H2O administration reveals impaired triglyceride storage in adipose tissue of insulin-resistant humans.

Journal of Lipid Research

Indirect evidence suggests that impaired triglyceride storage in the subcutaneous fat depot contributes to the development of insulin resistance via lipotoxicity. We directly tested this hypothesis by measuring, in vivo, triglyceride (TG) synthesis, de novo lipogenesis (DNL), adipocyte proliferation, and insulin-suppression of lipolysis in subcutaneous adipose tissue of BMI-matched individuals classified as insulin resistant (IR) or sensitive (IS). These results provide direct, in vivo evidence for impaired TG storage in subcutaneous adipose tissue of IR as compared with IS. Relative inability to store TG in the subcutaneous depot may represent a mechanism contributing to the development of insulin resistance in the setting of obesity.

Metabolic markers, regional adiposity, and adipose cell size: relationship to insulin resistance in African-American as compared with Caucasian women.

International Journal of Obesity

Understanding the Impact of Added Sugar Consumption on Risk for Type 2 Diabetes.

Journal of the California Dental Association

In vivo 2H2O administration reveals impaired triglyceride storage in adipose tissue of insulin-resistant humans.

Journal of Lipid Research

Indirect evidence suggests that impaired triglyceride storage in the subcutaneous fat depot contributes to the development of insulin resistance via lipotoxicity. We directly tested this hypothesis by measuring, in vivo, triglyceride (TG) synthesis, de novo lipogenesis (DNL), adipocyte proliferation, and insulin-suppression of lipolysis in subcutaneous adipose tissue of BMI-matched individuals classified as insulin resistant (IR) or sensitive (IS). These results provide direct, in vivo evidence for impaired TG storage in subcutaneous adipose tissue of IR as compared with IS. Relative inability to store TG in the subcutaneous depot may represent a mechanism contributing to the development of insulin resistance in the setting of obesity.

Metabolic markers, regional adiposity, and adipose cell size: relationship to insulin resistance in African-American as compared with Caucasian women.

International Journal of Obesity

Understanding the Impact of Added Sugar Consumption on Risk for Type 2 Diabetes.

Journal of the California Dental Association

Adipose cell size and regional fat deposition as predictors of metabolic response to overfeeding in insulin-resistant and insulin-sensitive humans.

Diabetes

Obesity is associated with insulin resistance (IR), but significant variability exists between similarly-obese individuals, pointing to qualitative characteristics of body fat as potential mediators. To test the hypothesis that obese, insulin-sensitive (IS) individuals possess adaptive adipose cell/tissue responses, we measured subcutaneous adipose cell size, insulin-suppression-of lipolysis, and regional fat responses to short-term overfeeding in BMI-matched overweight/obese individuals classified as IS or IR. At baseline, IR subjects exhibited significantly-greater visceral adipose tissue(VAT), intrahepatic lipid(IHL), plasma FFAs , adipose cell diameter, and %small adipose cells. With weight gain (3.1+1.4 kg), IR subjects demonstrated no significant change in adipose cell size, VAT, or insulin-suppression-of lipolysis, and only 8% worsening of insulin-mediated glucose uptake (IMGU).Alternatively, IS subjects demonstrated significant adipose cell enlargement, decrease in %small adipose cells, increase in VAT, IHL, lipolysis, 45% worsening of IMGU, and decreased expression of lipid metabolism genes. Smaller baseline adipose cell size and greater enlargement with weight gain predicted decline in IMGU, as did increase in IHL, VAT, and decrease in insulin-suppression-of lipolysis. Weight gain in IS humans causes maladaptive changes in adipose cells, regional fat distribution, and insulin resistance. The correlation between worsening insulin resistance and changes in adipose cell size, VAT, IHL, and insulin-suppression-of lipolysis highlight these factors as potential mediators between obesity and insulin resistance.

In vivo 2H2O administration reveals impaired triglyceride storage in adipose tissue of insulin-resistant humans.

Journal of Lipid Research

Indirect evidence suggests that impaired triglyceride storage in the subcutaneous fat depot contributes to the development of insulin resistance via lipotoxicity. We directly tested this hypothesis by measuring, in vivo, triglyceride (TG) synthesis, de novo lipogenesis (DNL), adipocyte proliferation, and insulin-suppression of lipolysis in subcutaneous adipose tissue of BMI-matched individuals classified as insulin resistant (IR) or sensitive (IS). These results provide direct, in vivo evidence for impaired TG storage in subcutaneous adipose tissue of IR as compared with IS. Relative inability to store TG in the subcutaneous depot may represent a mechanism contributing to the development of insulin resistance in the setting of obesity.

Metabolic markers, regional adiposity, and adipose cell size: relationship to insulin resistance in African-American as compared with Caucasian women.

International Journal of Obesity

Understanding the Impact of Added Sugar Consumption on Risk for Type 2 Diabetes.

Journal of the California Dental Association

Adipose cell size and regional fat deposition as predictors of metabolic response to overfeeding in insulin-resistant and insulin-sensitive humans.

Diabetes

Obesity is associated with insulin resistance (IR), but significant variability exists between similarly-obese individuals, pointing to qualitative characteristics of body fat as potential mediators. To test the hypothesis that obese, insulin-sensitive (IS) individuals possess adaptive adipose cell/tissue responses, we measured subcutaneous adipose cell size, insulin-suppression-of lipolysis, and regional fat responses to short-term overfeeding in BMI-matched overweight/obese individuals classified as IS or IR. At baseline, IR subjects exhibited significantly-greater visceral adipose tissue(VAT), intrahepatic lipid(IHL), plasma FFAs , adipose cell diameter, and %small adipose cells. With weight gain (3.1+1.4 kg), IR subjects demonstrated no significant change in adipose cell size, VAT, or insulin-suppression-of lipolysis, and only 8% worsening of insulin-mediated glucose uptake (IMGU).Alternatively, IS subjects demonstrated significant adipose cell enlargement, decrease in %small adipose cells, increase in VAT, IHL, lipolysis, 45% worsening of IMGU, and decreased expression of lipid metabolism genes. Smaller baseline adipose cell size and greater enlargement with weight gain predicted decline in IMGU, as did increase in IHL, VAT, and decrease in insulin-suppression-of lipolysis. Weight gain in IS humans causes maladaptive changes in adipose cells, regional fat distribution, and insulin resistance. The correlation between worsening insulin resistance and changes in adipose cell size, VAT, IHL, and insulin-suppression-of lipolysis highlight these factors as potential mediators between obesity and insulin resistance.

Efficacy and pharmacokinetics of subcutaneous exendin (9-39) in patients with post-bariatric hypoglycemia.

Diabetes Obes Metab

In vivo 2H2O administration reveals impaired triglyceride storage in adipose tissue of insulin-resistant humans.

Journal of Lipid Research

Indirect evidence suggests that impaired triglyceride storage in the subcutaneous fat depot contributes to the development of insulin resistance via lipotoxicity. We directly tested this hypothesis by measuring, in vivo, triglyceride (TG) synthesis, de novo lipogenesis (DNL), adipocyte proliferation, and insulin-suppression of lipolysis in subcutaneous adipose tissue of BMI-matched individuals classified as insulin resistant (IR) or sensitive (IS). These results provide direct, in vivo evidence for impaired TG storage in subcutaneous adipose tissue of IR as compared with IS. Relative inability to store TG in the subcutaneous depot may represent a mechanism contributing to the development of insulin resistance in the setting of obesity.

Metabolic markers, regional adiposity, and adipose cell size: relationship to insulin resistance in African-American as compared with Caucasian women.

International Journal of Obesity

Understanding the Impact of Added Sugar Consumption on Risk for Type 2 Diabetes.

Journal of the California Dental Association

Adipose cell size and regional fat deposition as predictors of metabolic response to overfeeding in insulin-resistant and insulin-sensitive humans.

Diabetes

Obesity is associated with insulin resistance (IR), but significant variability exists between similarly-obese individuals, pointing to qualitative characteristics of body fat as potential mediators. To test the hypothesis that obese, insulin-sensitive (IS) individuals possess adaptive adipose cell/tissue responses, we measured subcutaneous adipose cell size, insulin-suppression-of lipolysis, and regional fat responses to short-term overfeeding in BMI-matched overweight/obese individuals classified as IS or IR. At baseline, IR subjects exhibited significantly-greater visceral adipose tissue(VAT), intrahepatic lipid(IHL), plasma FFAs , adipose cell diameter, and %small adipose cells. With weight gain (3.1+1.4 kg), IR subjects demonstrated no significant change in adipose cell size, VAT, or insulin-suppression-of lipolysis, and only 8% worsening of insulin-mediated glucose uptake (IMGU).Alternatively, IS subjects demonstrated significant adipose cell enlargement, decrease in %small adipose cells, increase in VAT, IHL, lipolysis, 45% worsening of IMGU, and decreased expression of lipid metabolism genes. Smaller baseline adipose cell size and greater enlargement with weight gain predicted decline in IMGU, as did increase in IHL, VAT, and decrease in insulin-suppression-of lipolysis. Weight gain in IS humans causes maladaptive changes in adipose cells, regional fat distribution, and insulin resistance. The correlation between worsening insulin resistance and changes in adipose cell size, VAT, IHL, and insulin-suppression-of lipolysis highlight these factors as potential mediators between obesity and insulin resistance.

Efficacy and pharmacokinetics of subcutaneous exendin (9-39) in patients with post-bariatric hypoglycemia.

Diabetes Obes Metab

Integrative Human Microbiome Project: Dynamic Analysis of Microbiome-Host Omics Profiles during Periods of Human Health and Disease.

Cell Host Microbe

The Integrative Human Microbiome Project (iHMP, http://hmp2.org), the second phase of the NIH Human Microbiome Project, will study these interactions by analyzing microbiome and host activities in longitudinal studies of disease-specific cohorts and by creating integrated data sets of microbiome and host functional properties. These data sets will serve as experimental test beds to evaluate new models, methods, and analyses on the interactions of host and microbiome. Here we describe the three models of microbiome-associated human conditions, on the dynamics of preterm birth, inflammatory bowel disease, and type 2 diabetes, and their underlying hypotheses, as well as the multi-omic data types to be collected, integrated, and distributed through public repositories as a community resource.

In vivo 2H2O administration reveals impaired triglyceride storage in adipose tissue of insulin-resistant humans.

Journal of Lipid Research

Indirect evidence suggests that impaired triglyceride storage in the subcutaneous fat depot contributes to the development of insulin resistance via lipotoxicity. We directly tested this hypothesis by measuring, in vivo, triglyceride (TG) synthesis, de novo lipogenesis (DNL), adipocyte proliferation, and insulin-suppression of lipolysis in subcutaneous adipose tissue of BMI-matched individuals classified as insulin resistant (IR) or sensitive (IS). These results provide direct, in vivo evidence for impaired TG storage in subcutaneous adipose tissue of IR as compared with IS. Relative inability to store TG in the subcutaneous depot may represent a mechanism contributing to the development of insulin resistance in the setting of obesity.

Metabolic markers, regional adiposity, and adipose cell size: relationship to insulin resistance in African-American as compared with Caucasian women.

International Journal of Obesity

Understanding the Impact of Added Sugar Consumption on Risk for Type 2 Diabetes.

Journal of the California Dental Association

Adipose cell size and regional fat deposition as predictors of metabolic response to overfeeding in insulin-resistant and insulin-sensitive humans.

Diabetes

Obesity is associated with insulin resistance (IR), but significant variability exists between similarly-obese individuals, pointing to qualitative characteristics of body fat as potential mediators. To test the hypothesis that obese, insulin-sensitive (IS) individuals possess adaptive adipose cell/tissue responses, we measured subcutaneous adipose cell size, insulin-suppression-of lipolysis, and regional fat responses to short-term overfeeding in BMI-matched overweight/obese individuals classified as IS or IR. At baseline, IR subjects exhibited significantly-greater visceral adipose tissue(VAT), intrahepatic lipid(IHL), plasma FFAs , adipose cell diameter, and %small adipose cells. With weight gain (3.1+1.4 kg), IR subjects demonstrated no significant change in adipose cell size, VAT, or insulin-suppression-of lipolysis, and only 8% worsening of insulin-mediated glucose uptake (IMGU).Alternatively, IS subjects demonstrated significant adipose cell enlargement, decrease in %small adipose cells, increase in VAT, IHL, lipolysis, 45% worsening of IMGU, and decreased expression of lipid metabolism genes. Smaller baseline adipose cell size and greater enlargement with weight gain predicted decline in IMGU, as did increase in IHL, VAT, and decrease in insulin-suppression-of lipolysis. Weight gain in IS humans causes maladaptive changes in adipose cells, regional fat distribution, and insulin resistance. The correlation between worsening insulin resistance and changes in adipose cell size, VAT, IHL, and insulin-suppression-of lipolysis highlight these factors as potential mediators between obesity and insulin resistance.

Efficacy and pharmacokinetics of subcutaneous exendin (9-39) in patients with post-bariatric hypoglycemia.

Diabetes Obes Metab

Integrative Human Microbiome Project: Dynamic Analysis of Microbiome-Host Omics Profiles during Periods of Human Health and Disease.

Cell Host Microbe

The Integrative Human Microbiome Project (iHMP, http://hmp2.org), the second phase of the NIH Human Microbiome Project, will study these interactions by analyzing microbiome and host activities in longitudinal studies of disease-specific cohorts and by creating integrated data sets of microbiome and host functional properties. These data sets will serve as experimental test beds to evaluate new models, methods, and analyses on the interactions of host and microbiome. Here we describe the three models of microbiome-associated human conditions, on the dynamics of preterm birth, inflammatory bowel disease, and type 2 diabetes, and their underlying hypotheses, as well as the multi-omic data types to be collected, integrated, and distributed through public repositories as a community resource.

Plasma fatty acid ethanolamides are associated with postprandial triglycerides, ApoCIII, and ApoE in humans consuming a high-fructose corn syrup-sweetened beverage.

American Journal of Physiology, Endocrinology and Metabolism

In vivo 2H2O administration reveals impaired triglyceride storage in adipose tissue of insulin-resistant humans.

Journal of Lipid Research

Indirect evidence suggests that impaired triglyceride storage in the subcutaneous fat depot contributes to the development of insulin resistance via lipotoxicity. We directly tested this hypothesis by measuring, in vivo, triglyceride (TG) synthesis, de novo lipogenesis (DNL), adipocyte proliferation, and insulin-suppression of lipolysis in subcutaneous adipose tissue of BMI-matched individuals classified as insulin resistant (IR) or sensitive (IS). These results provide direct, in vivo evidence for impaired TG storage in subcutaneous adipose tissue of IR as compared with IS. Relative inability to store TG in the subcutaneous depot may represent a mechanism contributing to the development of insulin resistance in the setting of obesity.

Metabolic markers, regional adiposity, and adipose cell size: relationship to insulin resistance in African-American as compared with Caucasian women.

International Journal of Obesity

Understanding the Impact of Added Sugar Consumption on Risk for Type 2 Diabetes.

Journal of the California Dental Association

Adipose cell size and regional fat deposition as predictors of metabolic response to overfeeding in insulin-resistant and insulin-sensitive humans.

Diabetes

Obesity is associated with insulin resistance (IR), but significant variability exists between similarly-obese individuals, pointing to qualitative characteristics of body fat as potential mediators. To test the hypothesis that obese, insulin-sensitive (IS) individuals possess adaptive adipose cell/tissue responses, we measured subcutaneous adipose cell size, insulin-suppression-of lipolysis, and regional fat responses to short-term overfeeding in BMI-matched overweight/obese individuals classified as IS or IR. At baseline, IR subjects exhibited significantly-greater visceral adipose tissue(VAT), intrahepatic lipid(IHL), plasma FFAs , adipose cell diameter, and %small adipose cells. With weight gain (3.1+1.4 kg), IR subjects demonstrated no significant change in adipose cell size, VAT, or insulin-suppression-of lipolysis, and only 8% worsening of insulin-mediated glucose uptake (IMGU).Alternatively, IS subjects demonstrated significant adipose cell enlargement, decrease in %small adipose cells, increase in VAT, IHL, lipolysis, 45% worsening of IMGU, and decreased expression of lipid metabolism genes. Smaller baseline adipose cell size and greater enlargement with weight gain predicted decline in IMGU, as did increase in IHL, VAT, and decrease in insulin-suppression-of lipolysis. Weight gain in IS humans causes maladaptive changes in adipose cells, regional fat distribution, and insulin resistance. The correlation between worsening insulin resistance and changes in adipose cell size, VAT, IHL, and insulin-suppression-of lipolysis highlight these factors as potential mediators between obesity and insulin resistance.

Efficacy and pharmacokinetics of subcutaneous exendin (9-39) in patients with post-bariatric hypoglycemia.

Diabetes Obes Metab

Integrative Human Microbiome Project: Dynamic Analysis of Microbiome-Host Omics Profiles during Periods of Human Health and Disease.

Cell Host Microbe

The Integrative Human Microbiome Project (iHMP, http://hmp2.org), the second phase of the NIH Human Microbiome Project, will study these interactions by analyzing microbiome and host activities in longitudinal studies of disease-specific cohorts and by creating integrated data sets of microbiome and host functional properties. These data sets will serve as experimental test beds to evaluate new models, methods, and analyses on the interactions of host and microbiome. Here we describe the three models of microbiome-associated human conditions, on the dynamics of preterm birth, inflammatory bowel disease, and type 2 diabetes, and their underlying hypotheses, as well as the multi-omic data types to be collected, integrated, and distributed through public repositories as a community resource.

Plasma fatty acid ethanolamides are associated with postprandial triglycerides, ApoCIII, and ApoE in humans consuming a high-fructose corn syrup-sweetened beverage.

American Journal of Physiology, Endocrinology and Metabolism

Intervening in Early Childhood to Prevent Obesity: Best Practices for Home and Child Care Settings

Center for Weight and Health, UC Berkeley

An increasing proportion of U.S. children aged 2-5 are overweight. Early intervention among preschoolers at risk for poor nutrition and obesity, prior to the onset and consolidation of unhealthy eating habits and sedentary patterns, is critical to obesity prevention. Preschool aged children are more likely to modify their lifestyle behaviors than older children, as behaviors are less ingrained. Further, parents and other caregivers play a more central role in guiding younger children’s behaviors. Many children in this age group are in licensed child care during all or part of each week. Early childhood education settings can thus play an important part in providing opportunities for early development of healthy food and activity habits that are conducive to the maintenance of a healthy weight. Obesity prevention in young children is best done using a multi-component intervention program combining nutrition education, physical activity, and family support, with improved access to healthy food and exercise. Involving program participants in the development of programs is important to building acceptance by children, families, and communities. Demonstration of an effective public health approach to obesity prevention for very young children has the potential for wide dissemination for policy and practice and positive influence on the prevention of childhood obesity.

In vivo 2H2O administration reveals impaired triglyceride storage in adipose tissue of insulin-resistant humans.

Journal of Lipid Research

Indirect evidence suggests that impaired triglyceride storage in the subcutaneous fat depot contributes to the development of insulin resistance via lipotoxicity. We directly tested this hypothesis by measuring, in vivo, triglyceride (TG) synthesis, de novo lipogenesis (DNL), adipocyte proliferation, and insulin-suppression of lipolysis in subcutaneous adipose tissue of BMI-matched individuals classified as insulin resistant (IR) or sensitive (IS). These results provide direct, in vivo evidence for impaired TG storage in subcutaneous adipose tissue of IR as compared with IS. Relative inability to store TG in the subcutaneous depot may represent a mechanism contributing to the development of insulin resistance in the setting of obesity.

Metabolic markers, regional adiposity, and adipose cell size: relationship to insulin resistance in African-American as compared with Caucasian women.

International Journal of Obesity

Understanding the Impact of Added Sugar Consumption on Risk for Type 2 Diabetes.

Journal of the California Dental Association

Adipose cell size and regional fat deposition as predictors of metabolic response to overfeeding in insulin-resistant and insulin-sensitive humans.

Diabetes

Obesity is associated with insulin resistance (IR), but significant variability exists between similarly-obese individuals, pointing to qualitative characteristics of body fat as potential mediators. To test the hypothesis that obese, insulin-sensitive (IS) individuals possess adaptive adipose cell/tissue responses, we measured subcutaneous adipose cell size, insulin-suppression-of lipolysis, and regional fat responses to short-term overfeeding in BMI-matched overweight/obese individuals classified as IS or IR. At baseline, IR subjects exhibited significantly-greater visceral adipose tissue(VAT), intrahepatic lipid(IHL), plasma FFAs , adipose cell diameter, and %small adipose cells. With weight gain (3.1+1.4 kg), IR subjects demonstrated no significant change in adipose cell size, VAT, or insulin-suppression-of lipolysis, and only 8% worsening of insulin-mediated glucose uptake (IMGU).Alternatively, IS subjects demonstrated significant adipose cell enlargement, decrease in %small adipose cells, increase in VAT, IHL, lipolysis, 45% worsening of IMGU, and decreased expression of lipid metabolism genes. Smaller baseline adipose cell size and greater enlargement with weight gain predicted decline in IMGU, as did increase in IHL, VAT, and decrease in insulin-suppression-of lipolysis. Weight gain in IS humans causes maladaptive changes in adipose cells, regional fat distribution, and insulin resistance. The correlation between worsening insulin resistance and changes in adipose cell size, VAT, IHL, and insulin-suppression-of lipolysis highlight these factors as potential mediators between obesity and insulin resistance.

Efficacy and pharmacokinetics of subcutaneous exendin (9-39) in patients with post-bariatric hypoglycemia.

Diabetes Obes Metab

Integrative Human Microbiome Project: Dynamic Analysis of Microbiome-Host Omics Profiles during Periods of Human Health and Disease.

Cell Host Microbe

The Integrative Human Microbiome Project (iHMP, http://hmp2.org), the second phase of the NIH Human Microbiome Project, will study these interactions by analyzing microbiome and host activities in longitudinal studies of disease-specific cohorts and by creating integrated data sets of microbiome and host functional properties. These data sets will serve as experimental test beds to evaluate new models, methods, and analyses on the interactions of host and microbiome. Here we describe the three models of microbiome-associated human conditions, on the dynamics of preterm birth, inflammatory bowel disease, and type 2 diabetes, and their underlying hypotheses, as well as the multi-omic data types to be collected, integrated, and distributed through public repositories as a community resource.

Plasma fatty acid ethanolamides are associated with postprandial triglycerides, ApoCIII, and ApoE in humans consuming a high-fructose corn syrup-sweetened beverage.

American Journal of Physiology, Endocrinology and Metabolism

Intervening in Early Childhood to Prevent Obesity: Best Practices for Home and Child Care Settings

Center for Weight and Health, UC Berkeley

An increasing proportion of U.S. children aged 2-5 are overweight. Early intervention among preschoolers at risk for poor nutrition and obesity, prior to the onset and consolidation of unhealthy eating habits and sedentary patterns, is critical to obesity prevention. Preschool aged children are more likely to modify their lifestyle behaviors than older children, as behaviors are less ingrained. Further, parents and other caregivers play a more central role in guiding younger children’s behaviors. Many children in this age group are in licensed child care during all or part of each week. Early childhood education settings can thus play an important part in providing opportunities for early development of healthy food and activity habits that are conducive to the maintenance of a healthy weight. Obesity prevention in young children is best done using a multi-component intervention program combining nutrition education, physical activity, and family support, with improved access to healthy food and exercise. Involving program participants in the development of programs is important to building acceptance by children, families, and communities. Demonstration of an effective public health approach to obesity prevention for very young children has the potential for wide dissemination for policy and practice and positive influence on the prevention of childhood obesity.

Improvements in body fat distribution and circulating adiponectin by alternate-day fasting versus calorie restriction

The Journal of Nutritional Biochemistry

Calorie restriction (CR) and alternate-day fasting (ADF) beneficially affect several aspects of adipose tissue physiology, but direct comparisons between regimens have yet to be performed. The present study evaluated the effects of ADF versus CR on body fat distribution and circulating adiponectin levels and examined the kinetic mechanisms that underlie changes in fat distribution. Thirty female C57BL/6J mice were randomized to one of five groups for 4 weeks: (a) CR-25% (25% energy restriction daily), (b) ADF-75% (75% restriction on fast day), (c) ADF-85% (85% restriction on fast day), (d) ADF-100% (100% restriction on fast day) and (e) control (ad libitum fed). Body weights of the CR mice were lower than that of the ADF and control groups posttreatment. After 4 weeks of diet, the proportion of visceral fat decreased (P<.001) and the proportion of subcutaneous fat increased (P<.001) similarly in ADF and CR animals. Adiponectin increased (P<.05) by 62-86% in the ADF groups and by 69% in the CR group. Triglyceride (TG) synthesis and de novo lipogenesis were augmented (P<.05) in the subcutaneous fat pad of ADF and CR animals, relative to control. No differences in net lipolysis were observed, resulting in greater TG accumulation in the subcutaneous fat pad, with a shift in the ratio of TG between depots. These findings indicate that ADF (both modified and true) produces similar beneficial modulations in body fat distribution and adiponectin levels as daily CR.