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of Child Neurology

Treatment of Diabetes and Diabetic Complications With a Ketogenic Diet

Charles V. Mobbs, Jason Mastaitis, Fumiko Isoda and Michal Poplawski
J Child Neurol 2013 28: 1009 originally published online 16 May 2013
DOI: 10.1177/0883073813487596

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Special Issue Article
Journal of Child Neurology
28(8) 1009-1014
Treatment of Diabetes and Diabetic The Author(s) 2013
Reprints and permission:
Complications With a Ketogenic Diet DOI: 10.1177/0883073813487596

Charles V. Mobbs, PhD1, Jason Mastaitis, PhD1,

Fumiko Isoda, PhD1, and Michal Poplawski, MD, PhD1

Accumulating evidence suggests that low-carbohydrate, high-fat diets are safe and effective to reduce glycemia in diabetic patients
without producing significant cardiovascular risks. Most of these studies have been carried out specifically restricting carbohy-
drates, which tends to lead to increased protein intake, thus reducing the ketosis. However, diets that limit protein as well as
carbohydrates, entailing a composition very high in fat, appear even more effective to reduce glucose and whole-body glucose
metabolism in humans. In animal models, low-carbohydrate, high-protein diets do not produce ketosis or reduce glycemia but
rather cause obesity. However, limiting both protein and carbohydrates as in a classic ketogenic diet remarkably reduces blood
glucose in animal models of type 1 and type 2 diabetes and reverses diabetic nephropathy. Future studies should assess if ketogenic
diets would be effective to reverse diabetic complications in humans.

nephropathy, low carbohydrate, type 1 diabetes, type 2 diabetes mellitus

Received April 1, 2013. Accepted for publication April 1, 2013.

Low-Carbohydrate Diets in Humans was also matched to the standard diet (<1.7 g/kg/d), such that
the reduction in carbohydrate calories were entirely compen-
Before the discovery of insulin, the only effective treatment for
sated by an increase in fat, leading to a diet composed of about
diabetes mellitus was dietary restriction. An early description
85% fat. This diet was confirmed to be ketogenic: after the first
of the use of diet was by Allen, Stillman, and Fitz in 1919.1 The
week on the diet, all subjects exhibited detectable urinary
main focus at that time (when of course type 1 and type 2 dia-
ketones, whereas before the diet no urinary ketones were
betes were not distinguished) was to reduce body weight, usu-
detected.3 As will be discussed below, this was a key aspect
ally by an immediate fast to reduce acidosis and urinary of the study because in most popular low-carbohydrate diets
glucose. Protein was slowly introduced, then carbohydrate,
(e.g., the Atkins diet), reduced carbohydrate calories are
then fat. They also recommended periodic fasting, if possible
compensated by increased protein as well as increased fat, and
once per week, all with a view toward maintaining weight loss.
elevated protein intake attenuates or even blocks ketosis even
Generally their main concern was ketoacidosis, so the diet was
when carbohydrate intake is very low. In this study, 9 lean men
designed in part to avoid ketosis. Since the 1950s, weight loss
(4 of whom were athletes) were placed on a control diet for
for patients with type 2 diabetes was still recommended, along
baseline measurements, then switched to an isocaloric keto-
with diets low in fat and high in low-complex carbohydrate to
genic diet, as described above, in an inpatient highly controlled
reduce cardiovascular risks, but the evidence to support the use environment, for 4 weeks. The men were allowed to choose
of such diets was never as strong as the recommendations.
among meals prepared from ground beef, breast of chicken,
At about the time that insulin was discovered, thus reducing
tuna fish, egg solids, and cheddar cheese. Fats were in the form
the need for dietary therapies for diabetes, the ketogenic diet
was introduced to treat epilepsy, primarily if not exclusively
in children.2 In the ensuing decades, in the context of epilepsy,
short-term studies of the effects of the ketogenic diet were The Graduate School of the Icahn School of Medicine at Mount Sinai, New
carried out.2 However, surprisingly the first study of chronic York, NY, USA
metabolic effects of the ketogenic diet in humans appears to
Corresponding Author:
have been in 1983 by Phinney et al.3 This study is quite infor- Charles V. Mobbs, PhD, The Graduate School of the Icahn School of Medicine
mative. A key element of the study is that the diet was of course at Mount Sinai, One Gustave Levy Pl., New York, NY 10028, USA.
low carbohydrate (<20 g carbohydrate per day) but the protein Email: charles.mobbs@mssm.edu

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1010 Journal of Child Neurology 28(8)

of mayonnaise, heavy cream, sour cream, and cream cheese. intake (in contrast to the Phinney study, where caloric intake was
Ketosis was monitored daily, and all the men maintained keto- the same on both diets). Blood glucose and insulin levels were
genesis throughout the study, indicating excellent compliance. not reported so presumably did not change, in contrast to the
Consistent with the isocaloric diets, the slight weight loss on study by Phinney et al in lean individuals.3 Of particular note,
the ketogenic diet was not significant and could have been of the 41 subjects in the Westman study, 33 had moderate to
attributed to water loss. The most remarkable effects of the diet trace levels of urinary ketones. Even this modest level of
were reduction of blood glucose (after an overnight fast) by ketonuria is plausibly due to weight loss, which would be
about 15% and an even greater reduction (about 30%) in expected to increase ketonuria, raising the possibility that the
whole-body glucose metabolism, accompanied by an almost likely high-protein Atkins-type diet is not in itself directly keto-
doubling of plasma free fatty acids.3 genic (except perhaps for the 8 subjects with high urinary
Few studies extended this one for the next 2 decades, except ketones) but only ketogenic as an effect, rather than a cause,
the interesting study by Gumbiner et al.4 This small study (13 of weight loss. Furthermore, the lack of evidence of reduced
obese patients with type 2 diabetes; over only 6 weeks) was blood glucose or insulin on this diet is in contrast to the robust
designed primarily to assess if the ketosis that occurs conse- effects on a ketogenic diet. Nevertheless, these studies suggest
quent to weight loss is responsible for reduced hepatic glucose that by whatever mechanism, possibly simply by restricting food
output that accompanies weight loss in type 2 diabetic patients. choice, an Atkins-type low-carbohydrate, high-protein diet (rela-
To address this question, the authors implemented a very low tive to a classic ketogenic diet) facilitates weight loss.
calorie diet5 to induce weight loss, but one of the diets was A similar study the same year was carried out in women to
relatively high in carbohydrates, to reduce ketosis, whereas the assess the efficacy of an Atkins-type low-carbohydrate diet
other diet was very low in carbohydrates, which would enhance with otherwise ad lib intake (almost certainly involving
ketosis; caloric intake on both diets was controlled to be increased protein intake).8 This study also corroborates that
the same. However, the protein content was much higher than ad lib adherence to an Atkins-type low-carbohydrate diet does
for a normal diet (55%), which under normal caloric intake facilitate weight loss at least for 6 months, relative to a low-fat
would inhibit ketosis. Under the circumstances of equal (and diet in which caloric restriction was counseled. In this study
substantial) caloric restriction, both diets induced ketosis (even blood ketones were elevated after 3 months on the low-
though high in protein), but the high-carbohydrate diet reduced carbohydrate diet, but not after 6 months, again suggesting that
ketosis by about 60% compared to the low-carbohydrate diet increased ketosis was a result, not a cause, of the weight loss.
(as described below, we have observed a similar phenomenon A similar but larger (132 severely obese with 39% preva-
in mice). Under these conditions of equal and very low caloric lence of diabetes) and more definitive study was published the
intake, both diets induced apparently equal weight loss, but the next year by Sahama et al.9 This study was similarly naturalis-
low-carbohydrate diet produced lower blood glucose and tic as the study by Westman et al, but compared efficacy of a
improved glucose tolerance with no effect on plasma insulin, low-carbohydrate diet (in which both protein and fat were
and faster reduction in hepatic glucose output.4 Thus again this increased by choice of participants) to efficacy of a low-fat
study provides support for elevated ketosis improving glucose diet, in which participants were also specifically instructed to
control in diabetic patients independent of weight loss. reduce food intake (as per standard dietary counseling). This
The next significant study of the effect of low-carbohydrate study, also over a period of 6 months, clearly demonstrated that
diets in humans was a pilot study by Westman et al,6 which was a low-carbohydrate diet, without specific instructions to reduce
carried out to assess adherence to and efficacy of a low- caloric intake, was almost 3 times more effective to reduce
carbohydrate diet for 6 months. There were several key differ- body weight than the low-fat diet (5.8 vs 1.9 kg). Further-
ences between the study by Westman et al and that of Phinney more, the low-carbohydrate diet actually produced a greater
et al. First, the study by Phinney et al was a highly controlled reduction in triglycerides than the low-fat diet (38 vs 7
inpatient study in which caloric and protein intake were mg/dL), although plasma cholesterol was higher (2 vs 1
maintained as a constant, whereas the study by Westman et al mg/dL). Of particular interest, in diabetic patients the
implemented in a naturalistic out-patient framework, thus poten- low-carbohydrate diet reduced fasting blood glucose by 26%
tially more applicable to general practice, but also without compared to a reduction of only 5% on the low-fat diet; consis-
controlling protein or caloric intake. In fact the dietary plan was tent with the Westman study, the low-carbohydrate diet did not
essentially that of the Atkins diet7; since by 2002 the Atkins diet reduce fasting blood glucose in nondiabetic individuals. These
was highly popular, carrying out an assessment of the efficacy of studies support the possibility that a low-carbohydrate diet
the diet was quite timely. Second, the subjects in the study by might be particularly useful to reduce blood glucose in diabetic
Phinney et al were lean and even athletic, whereas the subjects patients. However, despite greater weight loss on the Atkins-
of in the study by Westman et al were overweight and obese and type low-carbohydrate diet, fasting blood glucose levels were
were motivated to lose weight. The main result of this study was similar in nondiabetic patients on the 2 diets.
that adherence to the low-carbohydrate diet led to weight loss A subsequent study by the Westman group assessed the
and, importantly, improved lipid profiles despite the relatively efficacy of the Atkins-type diet on hemoglobin A1c in type 2
high-fat diet. The weight loss entailed loss of both lean and fat diabetic patients.10 Of the 21 patients who completed the study,
mass, suggesting the weight loss was due to reduced caloric hemoglobin A1c was reduced from 7.5% to 6.3% (a both

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Mobbs et al 1011

statistically and clinically significant decrease). Diabetic lost weight (and normalized glucose homeostasis, including
medication was discontinued or decreased in most subjects, extreme reduction of both insulin and glucose) when placed
whereas triglycerides on the low-carbohydrate, high-fat diet on an even higher-fat but lower-carbohydrate (and lower
increased. Although the results of this study were impressive, protein) ketogenic diet. Of particular importance, this meta-
it is of some interest that of the 151 urine ketone measurements bolic normalization occurred without reducing caloric intake,
made during this study, only 27 were greater than trace, with 1 compared to the high-carbohydrate lower-fat diet. In fact, the
individual accounting for all 7 of the highest readings. It seems ketogenic diet induced increased oxygen consumption. These
plausible that the high ketosis in this individual may have been results are clearly consistent with the hypothesis that it is the
secondary to the most weight loss, but this particular informa- increase in ketones that drive this unique metabolic state.
tion is not indicated in the report. These studies corroborate that Interestingly, in a follow-up study, the same laboratory
the low-carbohydrate, high-protein Atkins-type diet produces demonstrated that the ketogenic diet fails to reduce body
beneficial effects to improve glucose control even though this weight in leptin-deficient ob/ob mice.13 Nevertheless the diet
diet in not robustly ketogenic in humans. On the other hand, the reduced blood glucose, associated with an induction of
Phinney et al study3 strongly suggests that a low-carbohydrate, FGF21,13 consistent with the studies of Phinney et al, who
low-protein diet is more robustly ketogenic and more robustly demonstrated reduced blood glucose and insulin, and reduced
reduces blood glucose and, possibly more importantly, reduce whole-body glucose utilization, without weight loss.3
whole-body glucose metabolism. As we will discuss below, Our laboratory carried out a similar study using the same Bio-
reduction of glucose metabolism is likely more important for serv diet and obtained essentially identical results,14 although
diabetic complications than reduction of blood glucose. our analysis was not as extensive as that of Kennedy et al.12
A study of some interest used a similar design, in which However, we carried out an additional study. Based on the
patients with type 2 diabetes were counseled to follow an different metabolic states that appeared to be produced by the
Atkins-type diet over a period of a year.11 Unfortunately, low-protein low-carbohydrate classic ketogenic diet used to treat
ketones were not measured, but weight loss was substantial epilepsy3 versus the high-protein low-carbohydrate diet
at the end of the year and, of particular interest, blood glucose promoted by Atkins and similar proponents, we developed a
was normalized after a year in diabetic patients with no effect high-protein version of the ketogenic diet, increasing the protein
of blood glucose in nondiabetic patients. These results further concentration to 20% and reducing the fat accordingly. In con-
support the value of the low-carbohydrate diet to treat type 2 trast to the ketogenic diet, this high-protein version was not keto-
diabetes. genic in mice under standard conditions. However, when surgery
The studies above generally support the idea that low- was performed on these mice (to allow monitoring of tempera-
carbohydrate diets may improve glucose control in type 2 ture by telemetry) and they lost weight as is usual after surgery,
diabetic patients without substantial increase in cardiovascular mice on the high-protein diet did exhibit higher levels of blood
risks. However, these improvements appear to be secondary to b-hydroxybutyric acid, consistent with the ketogenic effects of
weight loss, which is plausibly due at least in part to restricted the high-protein, low-carbohydrate diet during caloric restric-
dietary choices (though restricting carbohydrate clearly tion.9 Under standard ad lib fed conditions, in contrast to the
appears more protective than restricting fat). Because of the ketogenic diet, rather than reduce body weight, this diet
mechanistic limitations of human studies, animal studies were promoted weight gain and other obese phenotypes just as do
necessary to resolve these ambiguities. standard high-fat Western diets in mice.14 Furthermore,
despite low carbohydrate, blood glucose was not significantly
reduced, and in fact tended to increase as the mice gained
Low-Carbohydrate Diets in Animal Models of
weight. We were surprised by this and formulated a diet with
Obesity and Diabetes even lower carbohydrate to the lowest practical level (<1%) (and
Although the ketogenic diet had been studied in animal models increasing the fat accordingly). The effect of this diet was essen-
to clarify the mechanisms mediating the effects of the diet on tially the same as the previous high-protein diet; that is, the diet
epileptic seizures, relatively few studies had been carried out produced obesity as with other high-fat Western diets. When
to assess the effects of the diet on energy balance and glucose switched from the high-fat to the ketogenic diet, the mice rapidly
homeostasis until the seminal study by Kennedy et al.12 This lost weight without reducing caloric intake, and oxygen con-
study used the standardized commercial (Bio-serv) ketogenic sumption was induced within hours, before body composition
diet, modeled after the ketogenic diet used to treat epilepsy. changed. Together with the results of Kennedy et al12 in mice
This diet consists of 78.9% fat, 9.5% protein, and 0.76% carbo- and the studies of Phinney et al,3 these studies demonstrate that
hydrate (0% sucrose). Note that this closely models the diet of the low-carbohydrate, low-fat ketogenic diet does indeed
Phinney et al,3 which had an even greater percentage fat (85%), produce a unique metabolic state.12 We hypothesize that the
but the protein concentration is much lower than with the high-protein, low- (and very low) carbohydrate diets fail to
Atkins-type ad lib studies. This study documented the remark- reduce blood glucose and increase ketones because the excess
able metabolic effects of the demonstrable ketogenic diet, most protein is converted to glucose via gluconeogenesis.
importantly that mice made obese and prediabetic on a high- The efficacy of low-carbohydrate diets to reduce blood
fat, high-protein, high-carbohydrate Western diet rapidly glucose, especially in diabetic individuals, provides a major

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1012 Journal of Child Neurology 28(8)

rationale to treat patients with diabetes with such diets, in induction; that is, prior induction appeared to enhance sensitiv-
contrast to current recommendations, which advocate high- ity to the inducer. This would be analogous to genes induced by
carbohydrate low-fat diets.6,10 However, this rational may high glucose, like fibronectin25 or p65,28 maintaining induction
apply primarily to patients with type 2 diabetes, in which after returning to normal levels of glucose. However, a key
improvements in glucose homeostasis could be due primarily observation in this study was that if the concentration of the
to weight loss (at least in the high-protein form which is only inducer was sufficiently low, the lac operon would revert to its
weakly ketotic). For patients with type 1 diabetes there may previous uninduced state.26
be some concern that a ketogenic diet would promote ketoaci- These considerations led us to hypothesize that since a keto-
dosis, which could be potentially lethal. Much less research has genic diet not only reduces blood glucose to lower than normal
been done in patients with type 1 diabetes on low-carbohydrate levels, but more importantly reduces glucose metabolism, it
diets, but there is at least 1 case report of a patient with type 1 might be effective not only to prevent diabetic complications
diabetes and epilepsy who was treated with the classic (low- but to reverse them as well, which does not occur if blood
protein, low-carbohydrate) ketogenic diet to treat epilepsy.15 glucose is only normalized.17,21-23 To assess this hypothesis,
The diet produced robust ketogenesis and normalized glucose we initially assessed if mice with type 1 diabetes, untreated
and hemoglobin A1c. However after 15 months the child with insulin, would tolerate the diet or, perhaps, would suffer
refused the diet and was returned to a standard diet. This latter from exaggerated or even lethal ketoacidosis. This first study
observation indicates the potential difficulty of maintaining was carried out by Jodi Fox, MD, who was an endocrine fellow
adults, who have more choice in diet than children, on a classic and all too aware of this possibility. Thus, it was with some tre-
ketogenic diet. Therefore the promising results of the high- pidation that she placed a group of mice with streptozotocin-
protein low-carbohydrate diets may be more clinically relevant induced type 1 diabetes, average blood glucose over 500
for long-term maintenance. However, as described below, even mg/dL, on the ketogenic diet, not knowing if the next day she
short-term maintenance on the classic ketogenic diet may have might find them dead. They were not. Instead, the next day
an important role in therapy to reverse diabetic complications. their blood glucose levels had fallen from about 500 to about
Thus, one promising intervention would be to maintain diabetic 400 mg/dL, and every day their blood glucose continued to fall
patients long-term on an Atkins-type relatively high-protein by about 100 mg/dL, until the levels were approximately
diet, followed by a relatively short-term maintenance on a normal (100 mg/dL) despite insulinopenia. Thus, as is observed
ketogenic diet. in diabetic humans and ob/ob mice, the classic ketogenic diet is
Although reducing blood glucose in diabetic patients is of remarkably effective in normalizing blood glucose even in
course a major clinical goal, the main reason blood glucose highly hyperglycemic type 1 diabetic mice.
is of concern is the complications produced by high blood glu- We next assessed if the ketogenic diet would be effective in
cose, especially nephropathy, neuropathy, and retinopathy.16,17 reversing diabetic complications,29 which are not reversed
Diabetic complications are driven mainly by glucose metabo- even by normalization of blood glucose.17,21-23 We chose to
lism.18 As indicated above, Phinney et al demonstrated that a focus initially on nephropathy because this complication is rel-
ketogenic diet reduces whole-body glucose metabolism.3 atively easy to measure noninvasively by frequent assessment
Furthermore the effects of the ketogenic diet to reduce epileptic of urinary albumin/creatinine ratios. Because our goal was to
seizures are thought to be mediated at least in part by reducing reverse complications, not simply to prevent complications,
brain glucose metabolism.19 We have also directly demon- we monitored urinary albumin/creatinine ratios until they
strated in vitro that the ketone b-hydroxybutyrate blocks mole- clearly indicated nephropathy. The first study we carried out
cular effects of glucose.20 These considerations led us to was in type 1 diabetic mice produced by the Akita mutation,
hypothesize that a ketogenic diet, which of course increases in which insulin secretion is drastically reduced due to ER
blood levels of ketones and also decreases blood glucose, might stress in beta cells. After a 10-fold increase in albumin/creati-
prevent diabetic complications. nine ratios in the type 1 diabetic mice, half the mice were
Furthermore, a particular challenge with diabetic complica- placed on the ketogenic diet. As before, blood glucose in type
tions is that they resist reversal even when blood glucose in 1 diabetic mice was normalized within 1 week of placing the
normalized,21 a phenomenon referred to as metabolic mem- mice on the ketogenic diet; blood glucose was slightly but
ory.17,22,23 We had previously noted a similar phenomenon significantly reduced in wild-type controls. Within 2 weeks
with the hormone estradiol, which produces progressive neu- of the switch, 4 of 12 diabetic mice on chow had died, whereas
roendocrine effects that persist even after removal of estradiol, none of the mice on the ketogenic diet had died. Indeed all of
and hypothesized that glucose might produce similar persistent the diabetic mice on the ketogenic diet survived for 8 weeks
molecular effects that would be irreversible by normalizing (diabetic mice on the chow diet had been sacrificed for humane
glucose.24 This phenomenon was reported the next year.25 reasons), by which time their nephropathy (as indicated by
Subsequently, a fascinating paper appeared that demonstrated urinary albumin/creatinine ratios) had been completely
similar hysteretic behavior in the lac operon.26,27 These inves- reversed. The mice were then sacrificed and kidney gene
tigators demonstrated that after induction the lac operon expression was assessed. We developed a novel panel of stress
became persistently induced such that at levels of inducer pre- genes that were induced in association with diabetic nephropa-
viously insufficient to induce the operon, would now support thy, and they were all at least partially reversed (in most cases

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Mobbs et al 1013

completely reversed) by the ketogenic diet. We carried out a therapy in obese patients with non-insulin-dependent diabetes
similar study in type 2 (db/db) diabetic mice with the same mellitus. Am J Clin Nutr. 1996;63:110-115.
results: functionally (albumin/creatinine ratios) diabetic 5. Atkinson RL. Low and very low calorie diets. Med Clin North
nephropathy was completely reversed, and at the molecular Am. 1989;73:203-215.
level the gene profile associated with diabetic nephropathy was 6. Westman EC, Yancy WS, Edman JS, Tomlin KF, Perkins CE.
largely reversed as well.29 Effect of 6-month adherence to a very low carbohydrate diet
Taken together, these data suggest that a plausible treatment program. Am J Med. 2002;113:30-36.
for diabetic complications would be for patients to be placed on 7. Atkins R. Dr Atkins New Diet Revolution. New York, NY: Avon
a low-carbohydrate, high-protein diet Atkins-type diet,6,10 Books; 1998.
which entails relatively high compliance compared to the 8. Brehm BJ, Seeley RJ, Daniels SR, DAlessio DA. A randomized
classic ketogenic diet. After 6 months, patients would then be trial comparing a very low carbohydrate diet and a calorie-
placed on a classic ketogenic diet, monitoring relevant compli- restricted low fat diet on body weight and cardiovascular risk
cations (e.g., urinary albumin/creatine ratios). Once relevant factors in healthy women. J Clin Endocrinol Metab. 2003;88:
functions have been resolved, patients could then be returned 1617-1623.
to the Atkins-type diet, with the possibility that the transcrip- 9. Samaha FF, Iqbal N, Seshadri P, et al. A low-carbohydrate as
tional complexes involved have been reset. Clinical trials compared with a low-fat diet in severe obesity. N Engl J Med.
will be necessary to assess the efficacy of this strategy. 2003;348:2074-2081.
10. Yancy WS Jr, Foy M, Chalecki AM, Vernon MC, Westman EC. A
Acknowledgments low-carbohydrate, ketogenic diet to treat type 2 diabetes. Nutr
The animal work described herein was carried out at the Mount Sinai Metab (Lond). 2005;2:34.
School of Medicine. The authors acknowledge the work of Dr. Jodi 11. Dashti HM, Mathew TC, Khadada M, et al. Beneficial effects of
Fox, who initiated the studies using the ketogenic diet in diabetic ketogenic diet in obese diabetic subjects. Mol Cell Biochem.
mice. 2007;302:249-256.
12. Kennedy AR, Pissios P, Otu H, et al. A high-fat, ketogenic diet
Author Contributions induces a unique metabolic state in mice. Am J Physiol Endocri-
CVM conceived of the studies and wrote the manuscript; JM carried out nol Metab. 2007;292:E1724-E1739.
the initial studies using the ketogenic diet to reverse obesity in mice; FI 13. Badman MK, Kennedy AR, Adams AC, Pissios P, Maratos-Flier
assisted with all studies; MP carried out most of the studies using the
E. A very low carbohydrate ketogenic diet improves glucose tol-
ketogenic diet in diabetic mice, including molecular analysis.
erance in ob/ob mice independent of weight loss. Am J Physiol
Declaration of Conflicting Interests Endocrinol Metab. 2009;297:E1197-1204.
14. Mobbs CV, Mastaitis J, Yen K, et al. Low-carbohydrate diets
The authors declared no potential conflicts of interest with respect to
cause obesity, low-carbohydrate diets reverse obesity: a metabolic
the research, authorship, and/or publication of this article.
mechanism resolving the paradox. Appetite. 2007;48:135-138.
Funding 15. Dressler A, Reithofer E, Trimmel-Schwahofer P, et al. Type 1
diabetes and epilepsy: efficacy and safety of the ketogenic diet.
The authors disclosed receipt of the following financial support for the
research, authorship, and/or publication of this article: The studies Epilepsia. 2010;51:1086-1089.
described herein were funded by the Juvenile Diabetes Research 16. Keen H. The Diabetes Control and Complications Trial (DCCT).
Foundation. Health Trends. 1994;26:41-43.
17. Pop-Busui R, Herman WH, Feldman EL, et al. DCCT and EDIC
Ethical Approval studies in type 1 diabetes: lessons for diabetic neuropathy regard-
The studies described herein were approved by the Mount Sinai ing metabolic memory and natural history. Curr Diab Rep. 2010;
School of Medicine Institutional Animal Care and Use Committee 10:276-282.
( # 07-0044). 18. Brownlee M. Biochemistry and molecular cell biology of diabetic
complications. Nature. 2001;414:813-820.
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