Treatment of reactive hypoglycemia with the macrobiotic Ma-pi 2 diet as assessed by continuous glucose monitoring: The MAHYP randomized crossover trial

Soare, Andreea; Khazrai, Yeganeh Manon; Fontana, Lucia; Toro, Rossella Del; Lazzaro, Maria Concetta; Rosa, Claudia Di; Buldo, Antonia; Fioriti, Elvira; Maddaloni, Ernesto; Angeletti, Silvia; Mauro, A. Di; Gesuita, Rosaria; Skrami, Edlira; Tuccinardi, Dario; Fallucca, Sara; Pianesi, Mario; Pozzilli, Paolo

doi:10.1016/j.metabol.2017.01.023

Cited by 14 publications

(9 citation statements)

References 41 publications

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“…Therefore, we speculated that the HFD-induced early fasting hypoglycemia is mainly due to excessive insulin as a response to the HFD. Of note, studies have shown that a dietary fiber diet may reduce hypoglycemia by regulating the gut microbiota to reduce insulin secretion [17,18]. In this study, S. fusiforme polysaccharides were found to prevent HFD-induced early fasting hypoglycemia, which would be beneficial to people at a high risk of developing insulin-dependent diseases.…”

Section: Discussionmentioning

confidence: 64%

Sargassum fusiforme Polysaccharides Prevent High-Fat Diet-Induced Early Fasting Hypoglycemia and Regulate the Gut Microbiota Composition

Wei

Zhong

et al. 2020

Marine Drugs

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A low fasting blood glucose level is a common symptom in diabetes patients and can be induced by high-fat diet (HFD) feeding at an early stage, which may play important roles in the development of diabetes, but has received little attention. In this study, five polysaccharides were prepared from Sargassumfusiforme and their effects on HFD-induced fasting hypoglycemia and gut microbiota dysbiosis were investigated. The results indicated that C57BL/6J male mice fed an HFD for 4 weeks developed severe hypoglycemia and four Sargassumfusiforme polysaccharides (SFPs), consisting of Sf-2, Sf-3, Sf-3-1, and Sf-A, significantly prevented early fasting hypoglycemia without inducing hyperglycemia. Sf-1 and Sf-A could also significantly prevent HFD-induced weight gain. Sf-2, Sf-3, Sf-3-1, and Sf-A mainly attenuated the HFD-induced decrease in Bacteroidetes, and all five SFPs had a considerable influence on the relative abundance of Oscillospira, Mucispirillum, and Clostridiales. Correlation analysis revealed that the fasting blood glucose level was associated with the relative abundance of Mucispinllum and Oscillospira. Receiver operating characteristic analysis indicated that Mucispinllum and Oscillospira exhibited good discriminatory power (AUC = 0.745–0.833) in the prediction of fasting hypoglycemia. Our findings highlight the novel application of SFPs (especially Sf-A) in glucose homeostasis and the potential roles of Mucispinllum and Oscillospira in the biological activity of SFPs.

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Section: Discussionmentioning

confidence: 64%

Sargassum fusiforme Polysaccharides Prevent High-Fat Diet-Induced Early Fasting Hypoglycemia and Regulate the Gut Microbiota Composition

Wei

Zhong

et al. 2020

Marine Drugs

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“…In that respect it seems acceptable to require a stricter cut-off, such as 2.8 mmol/l rather than 3.3 mmol/l, for spontaneous events. In a study using continuous glucose monitoring on reactive hypoglycaemia, the cut-off for hypoglycaemia events was 70 mg/dl (3.9 mmol/l) 74 . In another study measuring continuous glycaemia in patients with reactive hypoglycaemia, a cut-off of 3.3 mmol/l (60 mg/dl) was used, but only 5% of symptom episodes were below this threshold 75 .…”

Section: : the Dumping Symptom Rating Scale Patient Selfassessment mentioning

confidence: 99%

International consensus on the diagnosis and management of dumping syndrome

Arts²,

et al. 2020

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Dumping syndrome is a frequent complication of cancer and non-cancer oesophageal and gastric surgery, as well as bariatric surgery (also known as metabolic surgery). These interventions change gastric anatomy and innervation, which can enable a considerable amount of undigested food to reach the small intestine too rapidly 1-4. Dumping syndrome comprises a constellation of symptoms that can be subdivided into early and late dumping syndrome symptoms, which can occur jointly or separately 1-8. Typically, symptoms of early dumping syndrome occur within the first hour after a meal and include gastrointestinal symptoms (abdominal pain, bloating, borborygmi, nausea and diarrhoea) and vasomotor symptoms (flushing, palpitations, perspiration, tachycardia, hypotension, fatigue, desire to lie down and, rarely, syncope) 1,2. The underlying mechanisms might involve osmotic effects, peptide hormone release and autonomic neural responses 1. Symptoms of late dumping syndrome usually occur between 1 and 3 h after a meal and are primarily the manifestations of hypoglycaemia, which mainly results from an incretin-driven hyperinsulinaemic response after carbohydrate ingestion. Hypoglycaemia-related symptoms are attributable to neuroglycopenia (which is indicated by fatigue, weakness, confusion, hunger and syncope) and to vagal and sympathetic activation (indicated by perspiration, palpitations, tremor and irritability) 1,2. The literature has referred to late dumping syndrome as 'reactive hypoglycaemia' or, after bariatric surgery, as 'postbariatric hypoglycaemia'. However, on the basis of a common pathophysiology of rapid exposure of the small intestine to nutrients, which is also seen in early dumping syndrome (see subsequent discussion), we refer to this phenomenon as 'late dumping syndrome'. The prevalence of dumping syndrome depends on the type and extent of surgery, and on the criteria used to diagnose dumping syndrome. Dumping syndrome occurs in approximately 20% of patients undergoing

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“…The macrobiotic Ma-Pi 2 diet reduced blood glucose excursions during the day, thereby facilitating glycemic control in subjects with RH. [48,49] Thus, these SCFA metabolites are preventive, reactive hypoglycemia.…”

Section: Gut Microbiomementioning

confidence: 99%

Postprandial Reactive Hypoglycemia

Altuntaş

2019

Sisli Etfal

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R eactive hypoglycemia (RH) is the condition of postprandially hypoglycemia occurring 2-5 hours after food intake. [1] Many conditions are associated with postprandial hypoglycemia. RH clinically seen in three different forms as follows: idiopathic RH (at 180 min), alimentary (within 120 min) and late RH (at 240-300 min). Earliest change before type 2 diabetes is the loss of first-phase insulin release, which emerges with fasting glucose levels of about 110 mg/dl. Lack of first-phase insulin release, an excellent predictor of both types of diabetes, is thought to be the earliest sign of the adverse effects of hyperglycemia on beta-cells and insulin-sensitive tissues. [2] When the first-phase insulin response decreases, firstly, blood glucose starts to rise after the meal, which leads to late but excessive secretion of the second-phase insulin secretion. Thus, late reactive hypoglycemia occurs. [3] Elevated insulin levels also cause downregulation of the insulin postreceptor on the muscle and fat cells, thus decreasing insulin sensitivity. The cause of the increase in insulin sensitivity in IRH at 3 h is not completely clear. However, there is a decrease in insulin sensitivity in late reactive hypoglycaemia at 4 or 5 hours. Thus, patients with hypoglycemia at 4 or 5 h who have those with a higher number of people with diabetes in the first-degree relative and who have obesity may be more susceptible to diabetes Reactive hypoglycemia (RH) is the condition of postprandially hypoglycemia occurring 2-5 hours after food intake. RH is clinically seen in three different forms as follows: idiopathic RH (at 180 min), alimentary (within 120 min), and late RH (at 240-300 min). When the first-phase insulin response decreases, firstly, blood glucose starts to rise after the meal. This leads to late but excessive secretion of the second-phase insulin secretion. Thus, late reactive hypoglycemia occurs. Elevated insulin levels also cause down-regulation of the insulin post-receptor on the muscle and fat cells, thus decreasing insulin sensitivity. The cause of the increase in insulin sensitivity in IRH at 3 h is not completely clear. However, there is a decrease in insulin sensitivity in late reactive hypoglycaemia at 4 or 5 hours. Thus, patients with hypoglycemia at 4 or 5 h who have a family history of diabetes and obesity may be more susceptible to diabetes than patients with hypoglycemia at 3 h. We believe that some cases with normal glucose tolerance in OGTT should be considered as prediabetes at <55 or 60 mg/dl after 4-5 hours after OGTT. Metformin and AGI therapy may be recommended if there is late RH with IFG. Also Metformin, AGİ, TZD, DPP-IVInhibitors, GLP1RA therapy may be recommended if there is late RH with IGT. As a result, postprandial RH (<55 or 60 mg/dl), especially after 4 hours may predict diabetes. Therefore, people with RH along with weight gain and with diabetes history in the family will benefit from a lifestyle modification as well as the appropriate antidiabetic approach in the prevention of diabetes.

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Treatment of reactive hypoglycemia with the macrobiotic Ma-pi 2 diet as assessed by continuous glucose monitoring: The MAHYP randomized crossover trial

Cited by 14 publications

References 41 publications

Sargassum fusiforme Polysaccharides Prevent High-Fat Diet-Induced Early Fasting Hypoglycemia and Regulate the Gut Microbiota Composition

Sargassum fusiforme Polysaccharides Prevent High-Fat Diet-Induced Early Fasting Hypoglycemia and Regulate the Gut Microbiota Composition

International consensus on the diagnosis and management of dumping syndrome

Postprandial Reactive Hypoglycemia

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