Katarina Borer
Research scholarship best describes my central career goal, occupation, and preoccupation during the past half of a century. My research explores the mechanisms of energy regulation, regulatory and nonhomeostatic, which partition nutrient energy among growth and stable adult body mass in response to exercise and its hormonal sequelae.I had the opportunity to study feeding and energy regulation in blowflies (with Dr. V. Dethier) rats (with Dr. A. Epstein), octopus, hamsters, and finally postmenopausal women. Among the more unusual findings of my research are growth acceleration and catch-up growth by voluntary exercise in mature hamsters, opportunistic feeding plan in Octopus briareus, increased insulin sensitivity in women after a single day of cutting carbohydrate intake by half, and increased anabolic bone markers in postmenopausal diabetic women if they exercise after eating but not before eating. Teaching at the University of Michigan between 1977 and 2018 was an integral part of my research scholarship: a stimulus for integration of facts, and a deductive starting point for laboratory experiments. I particularly valued guiding students in the strategies of doing research and teaching courses about regulated biological processes which require integration of diverse facts for full comprehension of function. The integrative process was put into action by writing Exercise Endocrinology (Human Kinetics 2003), Advanced Exercise Endocrinology (Human Kinetics 2013) and multiple reviews.
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Papers by Katarina Borer
Background
Postprandial hyperinsulinemia, hyperglycemia, and insulin resistance increase the risk of
type 2 diabetes (T2D) and cardiovascular disease mortality. Postprandial hyperinsulinemia
and hyperglycemia also occur in metabolically healthy subjects consuming high-carbohydrate
diets particularly after evening meals and when carbohydrate loads follow acute exercise.
We hypothesized the involvement of dietary carbohydrate load, especially when timed
after exercise, and mediation by the glucose-dependent insulinotropic peptide (GIP) in this
phenomenon, as this incretin promotes insulin secretion after carbohydrate intake in insulin-
sensitive, but not in insulin-resistant states.
Methods
Four groups of eight metabolically healthy weight-matched postmenopausal women were
provided with three isocaloric meals (a pre-trial meal and two meals during the trial day)
containing either 30% or 60% carbohydrate, with and without two-hours of moderate-intensity
exercise before the last two meals. Plasma glucose, insulin, glucagon, GIP, glucagonlike
peptide 1 (GLP-1), free fatty acids (FFAs), and D-3-hydroxybutyrate concentrations
were measured during 4-h postprandial periods and 3-h exercise periods, and their areas
under the curve (AUCs) were analyzed by mixed-model ANOVA, and insulin resistance
during fasting and meal tolerance tests within each diet was estimated using homeostasismodel
assessment (HOMA-IR).
Results
The third low-carbohydrate meal, but not the high-carbohydrate meal, reduced: (1) evening
insulin AUC by 39% without exercise and by 31% after exercise; (2) GIP AUC by 48%
without exercise and by 45% after exercise, and (3) evening insulin resistance by 37%
without exercise and by 24% after exercise. Pre-meal exercise did not alter insulin-,
PLOS ONE | DOI:10.1371/journal.pone.0165378 October 31, 2016 1 / 22
Conclusions
Evening postprandial insulin and GIP responses and insulin resistance declined by over
30% after three meals that limited daily carbohydrate intake to 30% compared to no such
changes after three 60%-carbohydrate meals, an effect that was independent of pre-meal
exercise. The parallel timing and magnitude of postprandial insulin and GIP changes
suggest their dependence on a delayed intestinal adaptation to a low-carbohydrate diet.
Pre-meal exercise exacerbated glucose intolerance with both diets most likely due to
impairment of insulin signaling by pre-meal elevation of FFAs.
Background
Postprandial hyperinsulinemia, hyperglycemia, and insulin resistance increase the risk of
type 2 diabetes (T2D) and cardiovascular disease mortality. Postprandial hyperinsulinemia
and hyperglycemia also occur in metabolically healthy subjects consuming high-carbohydrate
diets particularly after evening meals and when carbohydrate loads follow acute exercise.
We hypothesized the involvement of dietary carbohydrate load, especially when timed
after exercise, and mediation by the glucose-dependent insulinotropic peptide (GIP) in this
phenomenon, as this incretin promotes insulin secretion after carbohydrate intake in insulin-
sensitive, but not in insulin-resistant states.
Methods
Four groups of eight metabolically healthy weight-matched postmenopausal women were
provided with three isocaloric meals (a pre-trial meal and two meals during the trial day)
containing either 30% or 60% carbohydrate, with and without two-hours of moderate-intensity
exercise before the last two meals. Plasma glucose, insulin, glucagon, GIP, glucagonlike
peptide 1 (GLP-1), free fatty acids (FFAs), and D-3-hydroxybutyrate concentrations
were measured during 4-h postprandial periods and 3-h exercise periods, and their areas
under the curve (AUCs) were analyzed by mixed-model ANOVA, and insulin resistance
during fasting and meal tolerance tests within each diet was estimated using homeostasismodel
assessment (HOMA-IR).
Results
The third low-carbohydrate meal, but not the high-carbohydrate meal, reduced: (1) evening
insulin AUC by 39% without exercise and by 31% after exercise; (2) GIP AUC by 48%
without exercise and by 45% after exercise, and (3) evening insulin resistance by 37%
without exercise and by 24% after exercise. Pre-meal exercise did not alter insulin-,
PLOS ONE | DOI:10.1371/journal.pone.0165378 October 31, 2016 1 / 22
Conclusions
Evening postprandial insulin and GIP responses and insulin resistance declined by over
30% after three meals that limited daily carbohydrate intake to 30% compared to no such
changes after three 60%-carbohydrate meals, an effect that was independent of pre-meal
exercise. The parallel timing and magnitude of postprandial insulin and GIP changes
suggest their dependence on a delayed intestinal adaptation to a low-carbohydrate diet.
Pre-meal exercise exacerbated glucose intolerance with both diets most likely due to
impairment of insulin signaling by pre-meal elevation of FFAs.