A low-carbohydrate high-fat diet increases weight gain and does not improve glucose tolerance, insulin secretion or β-cell mass in NZO mice
BACKGROUND/OBJECTIVES: Dietary guidelines for the past 20 years have recommended that dietary fat should be minimized. In contrast, recent studies have suggested that there could be some potential benefits for reducing carbohydrate intake in favor of increased fat. It has also been suggested that low-carbohydrate diets be recommended for people with type 2 diabetes. However, whether such diets can improve glycemic control will likely depend on their ability to improve β-cell function, which has not been studied. The objective of the study was to assess whether a low-carbohydrate and therefore high-fat diet (LCHFD) is beneficial for improving the endogenous insulin secretory response to glucose in prediabetic New Zealand Obese (NZO) mice.
METHODS: NZO mice were maintained on either standard rodent chow or an LCHFD from 6 to 15 weeks of age. Body weight, food intake and blood glucose were assessed weekly. Blood glucose and insulin levels were also assessed after fasting and re-feeding and during an oral glucose tolerance test. The capacity of pancreatic β-cells to secrete insulin was assessed in vivo with an intravenous glucose tolerance test. β-Cell mass was assessed in histological sections of pancreata collected at the end of the study.
RESULTS: In NZO mice, an LCHFD reduced plasma triglycerides (P=0.001) but increased weight gain (P<0.0001), adipose tissue mass (P=0.0015), high-density lipoprotein cholesterol (P=0.044) and exacerbated glucose intolerance (P=0.013). Although fasting insulin levels tended to be higher (P=0.08), insulin secretory function in LCHFD-fed mice was not improved (P=0.93) nor was β-cell mass (P=0.75).
CONCLUSIONS: An LCHFD is unlikely to be of benefit for preventing the decline in β-cell function associated with the progression of hyperglycemia in type 2 diabetes.
| Errataetall: |
CommentIn: Nutr Diabetes. 2016 Jun 27;6:e214. - PMID 27348202 |
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| Medienart: |
E-Artikel |
| Erscheinungsjahr: |
2016 |
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| Erschienen: |
2016 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:6 |
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| Enthalten in: |
Nutrition & diabetes - 6(2016) vom: 15. Feb., Seite e194 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Lamont, B J [VerfasserIn] |
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| Links: |
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| Themen: |
97C5T2UQ7J |
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| Anmerkungen: |
Date Completed 22.09.2016 Date Revised 17.12.2018 published: Electronic CommentIn: Nutr Diabetes. 2016 Jun 27;6:e214. - PMID 27348202 Citation Status MEDLINE |
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| doi: |
10.1038/nutd.2016.2 |
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| Förderinstitution / Projekttitel: |
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| 100 | 1 | |a Lamont, B J |e verfasserin |4 aut | |
| 245 | 1 | 2 | |a A low-carbohydrate high-fat diet increases weight gain and does not improve glucose tolerance, insulin secretion or β-cell mass in NZO mice |
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| 500 | |a Date Revised 17.12.2018 | ||
| 500 | |a published: Electronic | ||
| 500 | |a CommentIn: Nutr Diabetes. 2016 Jun 27;6:e214. - PMID 27348202 | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a BACKGROUND/OBJECTIVES: Dietary guidelines for the past 20 years have recommended that dietary fat should be minimized. In contrast, recent studies have suggested that there could be some potential benefits for reducing carbohydrate intake in favor of increased fat. It has also been suggested that low-carbohydrate diets be recommended for people with type 2 diabetes. However, whether such diets can improve glycemic control will likely depend on their ability to improve β-cell function, which has not been studied. The objective of the study was to assess whether a low-carbohydrate and therefore high-fat diet (LCHFD) is beneficial for improving the endogenous insulin secretory response to glucose in prediabetic New Zealand Obese (NZO) mice | ||
| 520 | |a METHODS: NZO mice were maintained on either standard rodent chow or an LCHFD from 6 to 15 weeks of age. Body weight, food intake and blood glucose were assessed weekly. Blood glucose and insulin levels were also assessed after fasting and re-feeding and during an oral glucose tolerance test. The capacity of pancreatic β-cells to secrete insulin was assessed in vivo with an intravenous glucose tolerance test. β-Cell mass was assessed in histological sections of pancreata collected at the end of the study | ||
| 520 | |a RESULTS: In NZO mice, an LCHFD reduced plasma triglycerides (P=0.001) but increased weight gain (P<0.0001), adipose tissue mass (P=0.0015), high-density lipoprotein cholesterol (P=0.044) and exacerbated glucose intolerance (P=0.013). Although fasting insulin levels tended to be higher (P=0.08), insulin secretory function in LCHFD-fed mice was not improved (P=0.93) nor was β-cell mass (P=0.75) | ||
| 520 | |a CONCLUSIONS: An LCHFD is unlikely to be of benefit for preventing the decline in β-cell function associated with the progression of hyperglycemia in type 2 diabetes | ||
| 650 | 4 | |a Journal Article | |
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| 700 | 1 | |a Andrikopoulos, S |e verfasserin |4 aut | |
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