Depending on your severity, some meds including just probiotics can help.
From a part of a paper on RH.
Alpha Glucosidase Inhibitors
Inhibitors of α-glucosidase (acarbose and miglitol) can reduce the levels of GIP, which is released from K cells in the duodenum, which can be stimulated through the absorption of carbohydrates and fat. GIP increases significantly after the excessive ingestion of nutrients. There are studies that showed that he GIP and glucagon levels decreased after a mixed meal in patients with new diagnosed type 2 diabetics by treatment with single-dose acarbose[
36,
37] and acarbose decreased GIP and glucagon only in a mixed meal test rather than OGTT.[
38]
Glitazones
Low-dose glitazones given to patients with reactive hypoglycemia associated with IGT are also considered to be effective in the symptoms of reactive hypoglycaemia and the prevention of diabetes.[
39,
40] As a matter of fact, hyperinsulinemia and IGT were found in OGTT in 2 cases with hypoglycemic symptoms, and it has been shown that hyperinsulinemic clamp reduces the insulin sensitivity. In these cases, hypoglycaemic symptoms of IGT improved after the use of 15 mg pioglitazone. It has been reported that low dose of 15 mg pioglitazone prevents reactive hypoglycemia in impaired glucose tolerance.[
41]
Incretins
DPP-IV inhibitors have been suggested to be involved in the treatment of prediabetes.[
43] Glucagon levels decreased in GLP-1 compared to placebo and with a 32% reduction in postprandial glucose excursions no evidence of hypoglycemia or weight gain was seen in studies with single dose 50 mg vildagliptin. This effect suggests that it may be used in the treatment of reactive hypoglycaemia, possibly in prediabetic patients, and may prevent both the symptoms of hypoglycaemia and diabetes.[
44]
Dipeptidyl peptidase-4 (DPP-4) inhibitors improve insulin secretion and reduces glucagon secretion, thereby reducing hyperglycaemia. These incretin effects are glucose-dependent, thus minimize the risk of hypoglycaemia. Incretin-based therapies are of interest in subjects with mild postprandial glycaemic excursions but without overt T2DM. Sitagliptin treatment for 7–8 weeks resulted in reductions in post-challenge glucose excursions during both an MTT and an OGTT, in Japanese subjects with IGT. The observation that treatment with sitagliptin increased the early insulin response to the glucose load during the OGTT, and reduced circulating glucagon levels during the MTT.[
45]
It is suggested that the incretin-based treatments are promising in both IFG and IGT treatment, and we think that DPP-IV inhibitors may be useful in prediabetic patients, especially in postprandial reactive hypoglycaemia.[50] Also, GLP-1 receptor agonist is likely to have a preventive effect on postprandial reactive hypoglycemia with prediabetes, especially in overweight people. It has been suggested that pathophysiologic- based therapy is associated with marked improvement in glucose tolerance and reversion of prediabetes to normal glucose tolerance in more than 50% of patients.[
44-
47]
Gut Microbiome
Recently, the gut microbiota has been discussed as a potential target for the control of diabetes and reactive hypoglycaemia, and the possibility to correct gut microbiota dysbioses through diet. The macrobiotic Ma-Pi 2 diet, with its high fibre load, was effective in increasing the production of SCFAs by the gut microbiota. 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.