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Positive impact of gut adaptations after bariatric surgery Ribeiro-Parenti, Cavin and Le Gall 33

on intestinal adaptation in a Roux-en-Y bypass model. J
Pediatr Surg 2010, 45:987-995.
11. Mumphrey MB, Patterson LM, Zheng H, Berthoud H-R: Roux-enY gastric bypass surgery increases number but not density of
CCK-, GLP-1-, 5-HT-, and neurotensin-expressing
enteroendocrine cells in rats. Neurogastroenterol Motil 2013, 25:
12. Hansen CF, Bueter M, Theis N, Lutz T, Paulsen S, Dalbøge LS,
Vrang N, Jelsing J: Hypertrophy dependent doubling of L-cells
in Roux-en-Y gastric bypass operated rats. PLoS ONE 2013, 8:
13. Nerga˚rd BJ, Lindqvist A, Gislason HG, Groop L, Ekelund M,
Wierup N, Hedenbro JL: Mucosal glucagon-like peptide-1 and
glucose-dependent insulinotropic polypeptide cell numbers in
the super-obese human foregut after gastric bypass. Surg
Obes Relat Dis Off J Am Soc Bariatr Surg 2015, 11:1237-1246.
14. Cavin J-B, Couvelard A, Lebtahi R, Ducroc R, Arapis K, Voitellier E,
Cluzeaud F, Gillard L, Hourseau M, Mikail N et al.: Differences in
alimentary glucose absorption and intestinal disposal of blood
glucose after Roux-en-Y gastric bypass vs sleeve
gastrectomy. Gastroenterology 2016, 150 454–464.e9.
This paper provides a direct comparison of RYGB and VSG in intestinal
morphology and glucose transport in rats. In addition, the authors
demonstrated a direct role of the intestine in glucose handling after
RYGB both in rodents and in humans.
15. Mumphrey MB, Hao Z, Townsend RL, Patterson LM, Berthoud HR: Sleeve gastrectomy does not cause hypertrophy and
reprogramming of intestinal glucose metabolism in rats. Obes
Surg 2015, 25:1468-1473.
16. Dusaulcy R, Handgraaf S, Skarupelova S, Visentin F, Vesin C,
Heddad-Masson M, Reimann F, Gribble F, Philippe J, Gosmain Y:
Functional and molecular adaptations of enteroendocrine Lcells in male obese mice are associated with preservation of
pancreatic a-cell function and prevention of hyperglycemia.
Endocrinology 2016, 157:3832-3843.
This paper reconcile numerous conflicting reports about the increase or
decrease of number of enteroendocrine cells and enterohormone
response to a test meal in high fat diet obese mice. They show that
the increased GLP-1 cell number is not associated with an increased
GLP-1 secretion but may be rather a compensatory adaptation of L-cell
dysfunction in obesity.
17. Aranias T, Grosfeld A, Poitou C, Omar AA, Le Gall M, Miquel S,

Garbin K, Ribeiro A, Bouillot J-L, Bado A et al.: Lipid-rich diet
enhances L-cell density in obese subjects and in mice through
improved L-cell differentiation. J Nutr Sci 2015, 4:e22.
The present study shows for the first time that high fat/low carbohydrate
consumption increases L-cell density in the jejunum of morbidly obese
18. Psichas A, Reimann F, Gribble FM: Gut chemosensing
mechanisms. J Clin Invest 2015, 125:908-917.
19. Schmitt CC, Aranias T, Viel T, Chateau D, Le Gall M, WaligoraDupriet A-J, Melchior C, Rouxel O, Kapel N, Gourcerol G et al.:
Intestinal invalidation of the glucose transporter GLUT2 delays
tissue distribution of glucose and reveals an unexpected role
in gut homeostasis. Mol Metab 2017, 6:61-72.
20. Brown DX, Evans M: Choosing between GLP-1 receptor
agonists and DPP-4 inhibitors: a pharmacological
perspective. J Nutr Metab 2012, 2012:381713.
21. Zachos NC, Kovbasnjuk O, Foulke-Abel J, In J, Blutt SE, de
Jonge HR, Estes MK, Donowitz M: Human enteroids/colonoids
and intestinal organoids functionally recapitulate normal
intestinal physiology and pathophysiology. J Biol Chem 2016,
22. Zietek T, Rath E, Haller D, Daniel H: Intestinal organoids for
assessing nutrient transport, sensing and incretin secretion.
Sci Rep 2015, 5:16831.
23. Saeidi N, Meoli L, Nestoridi E, Gupta NK, Kvas S, Kucharczyk J,
Bonab AA, Fischman AJ, Yarmush ML, Stylopoulos N:
Reprogramming of intestinal glucose metabolism and
glycemic control in rats after gastric bypass. Science 2013,

24. Cavin J-B, Voitellier E, Cluzeaud F, Kapel N, Marmuse J-P,
Chevallier J-M, Msika S, Bado A, Le Gall M: Malabsorption and
intestinal adaptation after one anastomosis gastric bypass
compared with Roux-en-Y gastric bypass in rats. Am J Physiol
Gastrointest Liver Physiol 2016, 311:G492-G500.
25. Miyachi T, Nagao M, Shibata C, Kitahara Y, Tanaka N,
Watanabe K, Tsuchiya T, Motoi F, Naitoh T, Unno M:
Biliopancreatic limb plays an important role in metabolic
improvement after duodenal-jejunal bypass in a rat model of
diabetes. Surgery 2016, 159:1360-1371.
26. Pe´nicaud L, Hitier Y, Ferre´ P, Girard J: Hypoglycaemic effect of
metformin in genetically obese (fa/fa) rats results from an
increased utilization of blood glucose by intestine. Biochem J
1989, 262:881-885.
27. Bahler L, Stroek K, Hoekstra JB, Verberne HJ, Holleman F:

Metformin-related colonic glucose uptake; potential role for
increasing glucose disposal? A retrospective analysis of (18)FFDG uptake in the colon on PET-CT. Diabetes Res Clin Pract
2016, 114:55-63.
In this retrospectively analyze of 270 18F-FDG PET-CTs, the authors
report that metformin remained the strongest predictor for 18F-FDG
uptake in the intestine in multivariable analysis. This data suggest that
metformin use could increase intestinal glucose disposal in humans.
28. Bahler L, Holleman F, Chan M-W, Booij J, Hoekstra JB,
Verberne HJ: 18F-FDG uptake in the colon is modulated by
metformin but not associated with core body temperature and
energy expenditure. PLoS ONE 2017, 12:e0176242.
29. Gontier E, Fourme E, Wartski M, Blondet C, Bonardel G, Le
Stanc E, Mantzarides M, Foehrenbach H, Pecking A-P, Alberini JL: High and typical 18F-FDG bowel uptake in patients treated
with metformin. Eur J Nucl Med Mol Imaging 2008, 35:95-99.
30. McCreight LJ, Bailey CJ, Pearson ER: Metformin and the
gastrointestinal tract. Diabetologia 2016, 59:426-435.
31. Buse JB, DeFronzo RA, Rosenstock J, Kim T, Burns C, Skare S,
Baron A, Fineman M: The primary glucose-lowering effect of
metformin resides in the gut, not the circulation: results from
short-term pharmacokinetic and 12-week dose-ranging
studies. Diabetes Care 2016, 39:198-205.
32. Baud G, Daoudi M, Hubert T, Raverdy V, Pigeyre M, Hervieux E,
Devienne M, Ghunaim M, Bonner C, Quenon A et al.: Bile
diversion in Roux-en-Y gastric bypass modulates sodiumdependent glucose intestinal uptake. Cell Metab 2016, 23:547553.
33. Albaugh VL, Banan B, Ajouz H, Abumrad NN, Flynn CR: Bile acids

and bariatric surgery. Mol Aspects Med 2017
A recent extensive review on the modifications and contribution of bile
acids after bariatric surgeries to improved lipid and glucose homeostasis,
insulin sensitivity and energy expenditure.
34. Stearns AT, Balakrishnan A, Tavakkolizadeh A: Impact of Rouxen-Y gastric bypass surgery on rat intestinal glucose
transport. Am J Physiol Gastrointest Liver Physiol 2009, 297:
35. Bhutta HY, Deelman TE, Roux CWle, Ashley SW, Rhoads DB,
Tavakkoli A: Intestinal sweet-sensing pathways and metabolic
changes after Roux-en-Y gastric bypass surgery. Am J Physiol
Gastrointest Liver Physiol 2014, 307:G588-G593.
36. Magkos F, Bradley D, Eagon JC, Patterson BW, Klein S: Effect of

Roux-en-Y gastric bypass and laparoscopic adjustable
gastric banding on gastrointestinal metabolism of ingested
glucose. Am J Clin Nutr 2016, 103:61-65.
Using a mixed meal containing labeled [6,6-2H2]-glucose, the authors
demonstrated that GI clearance of ingested glucose is increased after
RYGB surgery. However, the difference effected by the bariatric procedure was low (from 10% 8% before to 15% 9% after surgery),
showing that intestinal glucose diversion during meals is not likely to
largely contribute to the postprandial improvement in glycemic control.
37. Ghani U: Re-exploring promising a-glucosidase inhibitors for
potential development into oral anti-diabetic drugs: finding
needle in the haystack. Eur J Med Chem 2015, 103:133-162.
38. Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D,
Neyrinck AM, Fava F, Tuohy KM, Chabo C et al.: Metabolic
Current Opinion in Pharmacology 2017, 37:29–34