scholarly journals Chronic exposure to free fatty acid reduces pancreatic beta cell insulin content by increasing basal insulin secretion that is not compensated for by a corresponding increase in proinsulin biosynthesis translation.

1998 ◽  
Vol 101 (5) ◽  
pp. 1094-1101 ◽  
Author(s):  
L C Bollheimer ◽  
R H Skelly ◽  
M W Chester ◽  
J D McGarry ◽  
C J Rhodes
Keyword(s):  
Insulin Secretion ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Beta Cell ◽  
Basal Insulin ◽  
Chronic Exposure ◽  
Pancreatic Beta Cell ◽  
Insulin Content ◽  
Proinsulin Biosynthesis ◽  
Basal Insulin Secretion

Effect of fatty acids on insulin release: role of chain length and degree of unsaturation

1994 ◽  
Vol 266 (4) ◽  
pp. E635-E639 ◽  
Author(s):  
E. C. Opara ◽  
M. Garfinkel ◽  
V. S. Hubbard ◽  
W. M. Burch ◽  
O. E. Akwari
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Fatty Acid ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Basal Insulin ◽  
Degree Of Unsaturation ◽  
Structural Differences ◽  
Basal Insulin Secretion

The purpose of the present study was to examine the role played by structural differences among fatty acids in their effect on insulin secretion by isolated perifused murine islets. Insulin secretion measured by radioimmunoassay was assessed either as total insulin output (ng.6 islets-1.20 min-1) or as percent of basal insulin secretion. Raising the glucose concentration from a basal 5.5 to 27.7 mM caused an increase of insulin output from 6.69 +/- 1.59 to 19.92 +/- 4.99 ng.6 islets-1.20 min-1 (P < 0.05) in control (untreated) islets. However, after 20-min exposure of islets to 5 mM 16:0 or 18:2, the effect of 27.7 mM glucose was enhanced or diminished, respectively. Basal insulin output (100% basal) changed to 44 +/- 10% basal (P < 0.005) with the addition of 5 mM 4:0 but was not altered when 4:0 was replaced by 6:0. Insulin output increased modestly with 5 mM 8:0 but significantly (P < 0.05) with 10:0 until a maximal of 280 +/- 24% basal with 12:0 (P < 0.01), then fell to 110 +/- 18 and 93 +/- 15% basal (P < 0.05) with 14:0 and 16:0, respectively. The addition of 5 mM 18:0 inhibited insulin secretion to 30 +/- 10% of basal (P < 0.003), and this effect was not caused by fatty acid interference with insulin assay.(ABSTRACT TRUNCATED AT 250 WORDS)

Relationship between insulin secretion, insulin content and dry weight of single rat pancreatic islets

1980 ◽  
Vol 94 (3) ◽  
pp. 365-370
Author(s):  
G. H. J. Wolters ◽  
W. Konijnendijk
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Outer Surface ◽  
Basal Insulin ◽  
Dry Weight ◽  
Insulin Content ◽  
Curvilinear Relationship ◽  
Rat Pancreatic Islets ◽  
Basal Insulin Secretion

Abstract. Single islets were incubated at glucose 5 mm for 60 min and subsequently at glucose 15 mm for 30 min. The insulin content of the incubated islets was proportional to the dry weight of the islets. The insulin secretion (Y) demonstrated a curvilinear relationship with the dry weight (X) of the islets, which could be described by the function Y = aX⅔ (a being a constant). On basis of this function it can be calculated that the insulin secretion of a particular islet is proportional to its outer surface. The consequence of this is that small sized islets secrete relatively much more insulin than large islets. Islets isolated with either purified or crude collagenase gave the same results except that a higher basal insulin secretion was observed with crude collagenase.

scholarly journals Pancreatic Thyrotropin Releasing Hormone and Mechanism of Insulin Secretion

2018 ◽  
Vol 50 (1) ◽  
pp. 378-384 ◽  
Author(s):  
Vladimír  Štrbák
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Basal Insulin ◽  
Thyrotropin Releasing Hormone ◽  
Insulin Content ◽  
Β Cells ◽  
Releasing Hormone ◽  
Rat Pancreatic Islets ◽  
Basal Insulin Secretion

Thyrotropin releasing hormone (TRH; pGlu-His-ProNH2) is expressed also in pancreatic β cells where it is colocalized in secretory granules with insulin. High perinatal changes of the TRH gene expression and TRH concentrations in rat pancreatic islets coincide with the perinatal maturation of the adequate insulin secretory responsiveness to glucose and other nutrient secretagogues. TRH secretion from pancreatic islets is stimulated by glucose and inhibited by insulin. Disruption of the TRH gene in knockout mice results in hyperglycemia accompanied by impaired insulin secretory response to glucose. Progress in understanding TRH - insulin relations may be substantial for improving knowledge of pathophysiological mechanisms included in changes of insulin secretion with possible clinical impact. Block of the last step of biosynthesis of α-amidated peptides, including TRH by disulfiram (DS) treatment of adult male rats subcutaneously with 200 mg/kg for five days in our experiments resulted in barely detectable levels of peptidyl-glycine α-amidating monooxygenase (PAM) in their pancreatic islets. TRH in physiological concentration (1 nM) does not affect basal insulin secretion from intact rat pancreatic islets. In contrast, basal insulin secretion from islets of DS-treated rats is four times higher compared to controls and could not be further stimulated by high-glucose. The addition of 1 nM TRH into medium decreased immediately basal insulin secretion in DS (TRH lacking) islets to control level and normalized also their response to glucose. Interestingly, absence of the secretory response to glucose in islets from TRH depleted rats was connected with their increase of insulin content during stimulation. Glucose stimulation together with 1 nM TRH normalized also insulin content in DS islets. Apparently, high insulin content in islets from TRH depleted animals is a result of block of regulatory secretion pathway redirected to constitutional secretion which was corrected by the addition of TRH. Type 2 diabetes mellitus is a disease characterized by various range from predominant insulin resistance with relative insulin deficiency to a predominant secretory defect with insulin resistance. These symptoms suggest a possible role of TRH dysregulation. In conclusion, presence of TRH in β cells ensures appropriate low basal (constitutive) insulin secretion. Release of TRH induced by glucose and possibly by other secretagogues has autocrine effect resulting in directing insulin secretion to regulatory pathway reacting to stimulation. If some defects of insulin secretion could be treated by TRH, various ways of applications (also oral and nasal) could be utilized. Moreover, positive side effects shown in animal experiments may accompany the treatment: TRH has the potential to prevent apoptosis and promotes insulin-producing cell proliferation and has also aging-reversing properties.

scholarly journals Beta-cell function improved by supplementing basal insulin secretion in mild diabetes.

BMJ ◽  
1976 ◽  
Vol 1 (6020) ◽  
pp. 1252-1254 ◽  
Author(s):  
R C Turner ◽  
S T McCarthy ◽  
R R Holman ◽  
E Harris
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Basal Insulin ◽  
Beta Cell Function ◽  
Cell Function ◽  
Mild Diabetes ◽  
Basal Insulin Secretion

scholarly journals What Is the Metabolic Amplification of Insulin Secretion and Is It (Still) Relevant?

Metabolites ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 355
Author(s):  
Ingo Rustenbeck ◽  
Torben Schulze ◽  
Mai Morsi ◽  
Mohammed Alshafei ◽  
Uwe Panten
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Adenine Nucleotides ◽  
Pancreatic Beta Cell ◽  
Secretory Response ◽  
Mitochondrial Activity ◽  
Insulin Synthesis ◽  
Sequence Of Events ◽  
Insulin Granules

The pancreatic beta-cell transduces the availability of nutrients into the secretion of insulin. While this process is extensively modified by hormones and neurotransmitters, it is the availability of nutrients, above all glucose, which sets the process of insulin synthesis and secretion in motion. The central role of the mitochondria in this process was identified decades ago, but how changes in mitochondrial activity are coupled to the exocytosis of insulin granules is still incompletely understood. The identification of ATP-sensitive K+-channels provided the link between the level of adenine nucleotides and the electrical activity of the beta cell, but the depolarization-induced Ca2+-influx into the beta cells, although necessary for stimulated secretion, is not sufficient to generate the secretion pattern as produced by glucose and other nutrient secretagogues. The metabolic amplification of insulin secretion is thus the sequence of events that enables the secretory response to a nutrient secretagogue to exceed the secretory response to a purely depolarizing stimulus and is thus of prime importance. Since the cataplerotic export of mitochondrial metabolites is involved in this signaling, an orienting overview on the topic of nutrient secretagogues beyond glucose is included. Their judicious use may help to define better the nature of the signals and their mechanism of action.

Pancreatic Beta-Cell Web: Its Possible Role in Insulin Secretion

Science ◽  
1972 ◽  
Vol 175 (4026) ◽  
pp. 1128-1130 ◽  
Author(s):  
L. Orci ◽  
K. H. Gabbay ◽  
W. J. Malaisse
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Pancreatic Beta Cell ◽  
Cell Web

38-OR: Deletion of the Mitofusins 1 and 2 (Mfn1 and Mfn2) from the Pancreatic Beta Cell Disrupts Mitochondrial Structure and Impairs Glucose-, but Not Incretin-, Stimulated Insulin Secretion

Diabetes ◽  
2021 ◽  
Vol 70 (Supplement 1) ◽  
pp. 38-OR
Author(s):  
ELENI GEORGIADOU ◽  
CHARANYA MURALIDHARAN ◽  
PAULINE L. CHABOSSEAU ◽  
ALEJANDRA TOMAS ◽  
THEODOROS STYLIANIDES ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Pancreatic Beta Cell ◽  
Mitochondrial Structure

Pancreatic beta-cell function and glucose metabolism in human segmental pancreas and kidney transplantation

1993 ◽  
Vol 264 (3) ◽  
pp. E441-E449 ◽  
Author(s):  
E. Christiansen ◽  
H. B. Andersen ◽  
K. Rasmussen ◽  
N. J. Christensen ◽  
K. Olgaard ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Beta Cell ◽  
Kidney Transplant ◽  
Beta Cell Function ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Secretion Rate ◽  
C Peptide ◽  
Insulin Secretion Rate

beta-Cell function and glucose metabolism were studied in eight insulin-dependent diabetic recipients of combined segmental pancreas and kidney transplant with peripheral insulin delivery (Px), in eight nondiabetic kidney-transplant individuals (Kx), and in eight normal subjects (Ns) after three consecutive mixed meals. All subjects had normal fasting plasma glucose, but increased basal levels of C-peptide were demonstrated in the transplant groups (P < 0.05 relative to Ns). Postprandial hyperglycemia was increased 14% in Kx and 32% in Px (P < 0.05), whereas compared with Ns postprandial C-peptide levels were increased three- and twofold, respectively, in Kx and Px (P < 0.05). Compared with Ns basal insulin secretion rate (combined model) was increased 2-fold in Kx and 1.4-fold in Px (P < 0.05). Maximal insulin secretion rate was reduced 25% in Px compared with Kx (P < 0.05) but not different from that of Ns (P NS). Also, maximal insulin secretion rate occurred later in Px than in controls (Tmax: Px 50 min, Kx 30 min, and Ns 32 min; P < 0.05). The total integrated insulin secretion was increased 1.4-fold in Px compared with Ns (P < 0.05) but decreased 1.4-fold compared with Kx (P < 0.05). Fasting and postprandial proinsulin-to-C-peptide molar ratios were inappropriately increased in Px compared with Kx and Ns. Basal hepatic glucose production was increased 43% in Px and 33% in Kx compared with Ns (P < 0.05). Postprandial total systemic glucose appearance was similar in all three groups, whereas peripheral glucose disposal was 15% reduced in Px (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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